Dissertations / Theses: 'Central nervous system in rats'

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Sevilla, Elenita L. "The influence of 5-HT3 receptor antagonism on aspects of CNS activity in morphine-dependent rats." Thesis, [Hong Kong] : University of Hong Kong, 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13019211.

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Silva, Kelly Regina Torres da. "Estudo da distribuição das proteínas relacionadas às teneurinas no sistema nervoso central de primatas não-humanos (Sapajus spp) e ratos (Rattus norvegicus)." Botucatu, 2016. http://hdl.handle.net/11449/139450.

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Orientador: Cláudio Aparecido Casatti
Resumo: As teneurinas (TENs) representam uma família de proteínas transmembrana preservada entre as espécies, presente principalmente no sistema nervoso central (SNC). Nos vertebrados essa família é composta por quatro homólogos, denominados de teneurina-1 a -4 (Ten-1, Ten-2, Ten-3 e Ten-4). Estudos mostraram a presença das TENs em vias motoras, olfatórias e visuais, especialmente durante a neurogênese em aves e roedores. A análise da distribuição neuroanatômica das TENs em primatas poderia ampliar o conhecimento destas proteínas, contribuindo com achados funcionais recentes. Portanto, os propósitos deste estudo foram: 1) avaliar a distribuição dos neurônios que exibem imunorreatividade relacionada às TENs-“like immunoreactivity” (TENs-LI), em particular Ten-2-LI, Ten-3-LI e Ten-4-LI no SNC do primata não-humano (Sapajus spp); 2) realizar análise comparativa dos sítios de distribuição da proteína Ten-3 entre o SNC de primatas (Sapajus spp) e roedores (Rattus norvegicus), uma vez que a Ten-3 apresentou distribuição significante no SNC de primatas; 3) correlacionar a distribuição das TENs com seus ligantes endógenos denominados de latrofilinas (LPHNs-1, 2 e 3) em áreas do SNC de primatas. Para isso, cortes coronais do SNC de macacos (n=3) e de ratos (n=4) foram submetidos à técnica de imuno-histoquímica e analisados em microscopia de luz ou confocal. Os resultados demonstraram a distribuição de neurônios e fibras nervosas exibindo TENs-LI em todo o neuroeixo de primatas. Neurônios e... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Teneurins (TENs) represent a transmembrane protein family preserved along animal species, mainly in the central nervous system (CNS). This protein family is constituted by four homologues, named as teneurin 1 to 4 (Ten-1, Ten-2, Ten-3 and Ten-4). Previous studies pointed out presence of TENs in motor, olfactory and visual systems in chicken and rodents, especially during neurogenesis. The neuroanatomic distribution analysis of TENs in the primate brain could provide additional information on this protein system, as well as support functional data from recent studies. Therefore, the purposes of the present study were: 1) to evaluate the distribution of neurons exhibiting TENs-like immunoreactivity (TENs-LI), in particular, Ten- 2-LI, Ten-3-LI and Ten-4-LI in the CNS of non-human primates (Sapajus spp); 2) to comparatively analyze the main brain regions exhibiting Ten-3-LI between primates (Sapajus spp) and rodents (Rattus norvegicus), since Ten-3-LI showed significant distribution in the CNS of primates; 3) To correlate TENsLI neurons with latrophilins (LPHNs-1, 2 and 3), an endogenous TENs ligand, in the CNS of primates. For this purpose, coronal histological sections of the CNS of non-human primates (n=3) and rats (n=4) were submitted to immunohistochemistry techniques and analyzed under light or confocal microscopes. Neurons and nerve fibers exhibiting TENs-LI were observed in all parts of the CNS in primates. Neurons showing Ten-2-LI were present mainly in the brainstem, s... (Complete abstract click electronic access below)
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Hughes, Rhome. "Immunohistochemical characterization of neuronal cilia in the rat central nervous system." Thesis, University of North Texas, 2002. https://digital.library.unt.edu/ark:/67531/metadc3136/.

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An anti-G"11 antibody was used to label neuronal cilia throughout the rat central nervous system. Immunoreactive cilia were observed in every examined region of the rat CNS, but not in monkey or mouse tissue. Antibodies to G"q and G"q/11 failed to label cilia. Immunoreactive cilia were observed as early as postnatal day 0 in spinal tissue, and postnatal day 3 in hypothalamic tissue. There was a statistically significant negative correlation between a region's mean cilium length and that region's distance to the nearest ventricle; regions nearest ventricles were those with the longest cilia. This correlation suggests neuronal cilia may function as chemosensors, detecting substances as they move out from the cerebrospinal fluid and into the extracellular space of the brain.

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McClure-Sharp, Jilliane Mary, and mikewood@deakin edu au. "Regulation of corticotropin-releasing factor concentration and overflow in the rat central nervous system." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060802.143911.

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Corticotropin-releasing factor (CRF) is the primary hormone of the hypothalamo-pituitary adrenal axis (HPA-axis). In addition to its endocrine function, it has been proposed that CRF acts as a neurotransmitter. The widespread distribution of CRF immunoreactivity and CRF receptors in the rat central nervous system (CNS) supports this theory. Immunohistochemical studies have demonstrated high levels of CRF immunoreactivity the rat hypothalamus, a brain region involved in the regulation and integration of a variety of endocrine and autonomic homeostatic mechanisms. CRF has been shown to be involved in a number of these activities such as blood pressure control, food and water intake, behaviour and emotional integration. Many of these activities demonstrate progressive dysfunction as ageing proceeds. The aim of this thesis was to investigate the regulation of CRF in the rat CNS, particularly over the period of maturation and ageing. Tissue extraction and peptide radioimmunoassay (RIA) techniques were developed in order to measure regional CRF concentrations as a function of age in the rat CNS. Seven brain regions were examined including the hypothalamus, pituitary, medulla oblongata, pons, cerebral cortex, cerebellum and midbrain. Three age ranges were investigated: 3 4 weeks, 4 5 months and 14 18 months, representing young, mature and old age groups. Data for the tissues of individual rats from each age group were analysed using one-way analysis of variance (ANOVA) with post-hoc Scheffé tests (SPSS Release 6 for Windows, 1989 1993). CRF were detected in measurable quantities in all brain regions examined. Different age-related patterns of change were observed in each brain region. CRF concentrations (ng/g tissue) were highest in the pituitaries of young rats and were significantly reduced over the period of maturation (P< 0.05). However, the high CRF concentration of the young rat pituitary was likely to be a factor of the smaller tissue mass. Although the absolute CRF content (ng/tissue) of this tissue appeared to decline with maturation and ageing, the reduction was not significant (P>0.05). Therefore the pituitary of the young rat was relatively enriched with CRF per gram tissue. The highest CRF concentration in mature and aged rats was measured in the hypothalamus, in accordance with previous immunohistochemical studies. Hypothalamic CRF concentrations (ng/g tissue) demonstrated no significant alterations with maturation and ageing. The absolute CRF content (ng/tissue) of the hypothalamus was significantly less in the young rat compared to mature and aged animals, however this was accompanied by a smaller tissue mass (P<0.05). The CRF concentrations (ng/g tissue) of the rat cerebral cortex and medulla oblongata demonstrated significant reduction with advancing age (P<0.05), however in both cases this appeared to be due to significant increases in mean tissue mass. The absolute CRF content of these tissues (ng/tissue) were not significantly different over the period of maturation and ageing (P>0.05). CRF concentration (ng/g tissue) and absolute content (ng/tissue) of the pons demonstrated a trend to increase with advanced age in the rat, however this was not significant in both cases (P>0.05). Of interest were the significant increases observed in the CRF concentrations of the cerebellum and midbrain (ng/g tissue with advanced ageing (P<0.05). Significant increases were also observed in the mean tissue mass and absolute CRF content (ng/tissue) of these regions in aged rats (P<0.05). These findings perhaps indicate increased CRF synthesis and or decreased CRF turnover in these tissues with advancing age. The second stage of these studies examined age-related alterations in basal and potassium-stimulated hypothalamic CRF and overflow over the period of maturation and ageing in the rat, and required the preliminary development of an in vitro tissue superfusion system. The concomitant release of the co-modulatory compound, neuropeptide Y (NPY) was also measured. NPY has been shown to positively regulate CRF release and gene expression in the hypothalamus. In addition, NPY has been demonstrated to be involved in a number of hypothalamic activities, including blood pressure control and food intake regulation. Hypothalamic superfusion data were analysed using one factor repeated measures ANOVA (SPSS Release 6 for Windows, 1989-1993) followed by least significant difference tests ( Snedecor and Cochran, 1967) to enable both time and age comparisons. Basal hypothalamic CRF overflow was unaltered with maturation and ageing in the rat. Potassium stimulation (56 mM) elicted a significant 2 3 fold increase in hypothalamic CRF overflow across age groups (P<0.05). Stimulated hypothalamic CRF overflow was significantly greater in the young rat compared to the mature and aged animals (P<0.05). The enhanced response to depolarizing stimulus was observed at an age when the absolute CRF content of the hypothalamus was significantly less that of other age groups. It is possible that the enhanced responsiveness of the young rat may be of survival advantage in life threatening situations. Basal hypothalamic NPY overflow was much less than that of CRF, and potassium stimulation resulted in a very different age-related profile. The hypothalamic NPY response to depolarization was significantly reduced in the young rat and declined significantly with advanced ageing (P<0.05). The contrasting profiles of stimulated CRF and NPY overflow may indicate the activity of alternative regulatory factors present in the hypothalamus, whose activity may also be affected in an age-related manner. The final stage of these studies examined the nature of NPY modulation of hypothalamic CRF overflow in the mature rat. The facilitatory effect of NPY on hypothalamic CRF overflow was confirmed. The application of NPY (0.1 µM) significantly increased CRF overflow approximately 4 fold of basal (P<0.05). In addition, the role of the NPY-Y1 receptor was investigated by the prior application of Y1 receptor antagonists, GW1229 (0.05 µM). At this concentration GW1229 significantly reduced hypothalamic CRF overflow induced by perfusion with NPY (0.1 µm), P<0.05. It was concluded the Y1 receptor does have a role in the regulation of hypothalamic CRF overflow by NPY.

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Davies, M. "5-hydroxytryptamine receptors in the central nervous system." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382505.

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Yick, Leung-wah. "Promotion of neuronal survival and axonal regeneration in Clarke's nucleus after spinal cord injury in adult rats /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21090099.

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Alrtemi, Milod M. Ahmed. "Radioprotective effects of rooibos herbal tea on the developing central nervous system of wistar rats." University of the Western Cape, 2018. http://hdl.handle.net/11394/6532.

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Magister Scientiae - MSc
Background: Early postnatal radiation exposure from environmental, diagnostic or therapeutic sources is potentially deleterious to the developing nervous system resulting in oxidative stress, structural damage, altered neurochemistry, DNA damage, inflammatory stresses as well as correlating cognitive impairment during adult life. Numerous studies in literature have investigated the radioprotective effects of medicinal plants and beverages. However, only a few studies have focused on the radioprotective effects of rooibos, an indigenous South African herbal tea, well known for its many acclaimed health benefits. Aims: This study was done to investigate the diverse radioprotective potential of fermented Rooibos herbal tea (FRHT) consumed ad libitum by pregnant rats on the adult offspring rats exposed to a once-off 6 Gy dose of gamma irradiation on postnatal day 3. Methods: Twenty-four (24) adult female rats were equally divided into four groups (6 per group) as control (NS), radiation (X), tea (RT) and their combination. On PND 30, offspring rats were subjected to neurobehavioural assessment for open field and novel object recognition parameters and later sacrificed, the brain tissues removed and processed for histological, immunohistochemical and neurochemical analyses, using standard techniques. Results: Pre-treatment with FRHT showed overall protection against radiation-induced distortions in offspring rats by significantly improving exploratory activity, the frequency of central square entry, rearing episodes, cumulative freezing time and memory retention as indicated by a relatively higher recognition index. FRHT was also found to significantly improve the antioxidant defence mechanisms in the offspring rats by reversing lowered FRAP levels, increasing superoxide dismutase and catalase enzyme activities and reducing lipid peroxidation. Histological and immunohistochemical analyses showed that morphological alterations were generally attenuated in the RTX group and the high number of caspase-3 and Glial fibrillary acidic protein (GFAP)-positive cells was significantly reduced, indicating protective effects against apoptosis and gliosis. Conclusion: Taken together, our findings tend to suggest that the potential radioprotective effects of FRHT are multimodal, possibly executed through the anti-apoptotic, antioxidative, anti-gliosis and other mechanisms, as observed in this study, and this is often attributed to the high polyphenol content in Rooibos tea.

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Totola, Leonardo Tedesco. "Envolvimento da região comissural do núcleo do trato solitário nas respostas cardiovasculares e simpáticas promovidas pela injeção do anti-hipertensivo de ação central moxonidina em ratos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-14032014-130320/.

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O objetivo central do presente estudo foi avaliar se os agonistas adrenérgicos a2 e imidazólicos, importantes drogas de ação anti-hipertensiva utilizadas na clínica médica, podem atuar também na região comissural do núcleo do trato solitário (NTSc), o qual constituí uma importante região do bulbo envolvida no controle cardiovascular. Em ratos Wistar adultos, observamos que a hipotensão produzida pela injeção de moxonidina no 4º V foi reduzida após a lesão eletrolítica do NTSc. Ademais, a injeção de moxonidina no NTSc reduziu a pressão arterial média (PAM), a frequência cardíaca (FC) e a atividade simpática (AS). A injeção de antagonistas adrenérgicos (ioimbina ou RX821002) no NTSc foi capaz de bloquear as respostas hipotensora e de simpatoinibição produzida pela moxonidina no NTSc. A injeção bilateral de moxonidina na região RVL/C1 reduziu PAM e AS de maneira mais intensa do que as injeções no NTSc. Em concordância com os resultados apresentados, mostramos que a atividade elétrica dos neurônios da região do RVL/C1 foi reduzida após a injeção de moxonidina no NTSc. Concluímos que a moxonidina pode produzir os seus efeitos anti-hipertensivos atuando também sobre o NTSc.
The main objective of this study was to evaluate whether the a2 adrenergic and imidazoline agonists, important antihypertensive drugs used in clinical medicine, may also act in the commissural region of the nucleus of the solitary tract (cNTS), which constitutes an important region of brainstem involved in cardiovascular control. In adult rats, the hypotension elicited by central injections of moxonidine was reduced after electrolytic lesion of cNTS. Furthermore, injection of moxonidine into the cNTS reduced mean arterial pressure (MAP), heart rate (HR) and sympathetic activity (SNA). Injection of the a2 adrenergic antagonist (RX821002 or yohimbine) into the cNTS completely blocked the hypotension and sympathoinhibition responses produced by moxonidine into the cNTS. Bilateral injection of moxonidine in the RVLM/C1 produced huge effects on MAP and SNA in comparison of cNTS injections. In agreement with our results, moxonidine-injected into the cNTS also elicited a reduction in the activity of RVLM/C1 neurons. Our conclusion is that moxonidine may produce their antihypertensive effects also acting on cNTS neurons.

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Pook, P. C. K. "Ligand binding and electrophysiological studies of excitatory amino acid receptors in the rat central nervous system." Thesis, University of Bristol, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381675.

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Hu, Ying. "Optic nerve regeneration in adult rat /." Connect to this title, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0080.

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Graca, D. L. "Investigation into ethidium bromide demyelination in the central nervous system." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373675.

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Dyck, Richard Henry. "Cytochrome oxidase histopathology in the central nervous system of developing rats displaying methylmercury-induced movement and postural disorders." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27873.

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Sprague-Dawley rats were administered daily, subcutaneous injections of methylmercuric chloride at a dose of 5 mg/Hg/kg beginning on postnatal day 5. By their fourth postnatal week, animals exhibited a constellation of neurological signs of motor impairment which resembled the cerebral palsy syndrome of humans perinatally exposed to methylmercury. Routine histological examination of the brain revealed no gross differences between methylmercury-treated (MeHg), normal control (NC) or weight-matched littermates. The histochemical localization of the mitochondrial enzyme cytochrome oxidase (CO) was utilized in Experiment I to examine possible alterations in the metabolic activity of motor nuclei which might contribute to the observed movement and postural disorders. A population of intensely-staining cytochrome oxidase neurons (ICONs) in the magnocellular portion of the red nucleus (RMC) and interrubral mesencephalon (IRM) were conspicuously present in all MeHg animals at the onset of motor impairment. These morphologically, histochemically, and anatomically distinct neurons did not exhibit intense CO staining in control animals. Conversely, a significant decrease was demonstrated in the oxidative metabolic activity of many neurons in the substantia nigra, zona reticulata of MeHg animals. In Experiment II, the postnatal appearance of ICONs was morphometrically quantified in MeHg animals sacrificed at PND 14, 16, 18, 20, 22, or 25. The histochemically-defined onset of increased metabolic activity in ICONs was first observed on PND 16, at least one week before the onset of clinical signs of neurological impairment. This was the earliest manifestation of methylmercury neurotoxicity yet described in this animal model. A subsequent four-fold increase in the total number of ICONs at PND 18 was followed by a gradual decrease in number to PND 25. Significantly more of the ICONs were found in the IRM than in the RMC at PND 18 & 20. The possibility that the increased activity of ICONs may result from disinhibition of specific afferents to the red nucleus was addressed by introducing either hemidecortication or hemicerebellectomy on PND 10 and then morphometrically determining the deviation from symmetry in the bilateral distribution of the total number of ICONs in the RMC and IRM at PND 22. The distribution of ICONs was symmetrical and not different in either hemidecorticate or unoperated controls. A significant (36%) decrease in the total number of ICONs was observed in both the RMC and IRM contralateral to hemicerebellectomy. The identical ipsilateral regions did not differ from control or hemidecorticate MeHg animals. In Experiment III, the anatomical distribution of major histocompatability complex antigens (MHC) in the brain of MeHg animals was examined using immunohistochemical methods. MHC immunoreactivity was widely distributed throughout the brain of MeHg animals. Areas with low immunoreactivity, or lack of it, stand out and include all of the hippocampus, thalamus, pyriform and entorhinal cortex, and lateral cerebellar hemispheres. Moderate staining intensity was observed in neocortical areas, basal forebrain, caudate-putamen and cerebellar vermis. Strong immunoreactivity was found in red nucleus, substantia nigra, cingulate cortex, retrosplenial cortex, presubiculum, parasubiculum and vestibular nuclei. It was suggested that the increased activity of ICONs likely contributes to the movement and postural disorders resulting from methylmercury intoxication. The increased activity in ICONs was determined to be, at least partially, dependent upon cerebellar input. The results are discussed with reference to the toxic effects of methylmercury and specifically to the susceptibility of GABAergic interneurons in perinatal trauma. Possible analogies are drawn between the mechanisms of methylmercury-induced cerebral palsy syndrome and those of other developmental movement and postural disorders.
Medicine, Faculty of
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Czajkowski, Laura Anne. "Classical Conditioning and Immune Reactivity in Rats." DigitalCommons@USU, 1988. https://digitalcommons.usu.edu/etd/5606.

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Psychoneuroimmunology is an interdisciplinary area that examines the interaction between behavior, the central nervous system, and the immune system. Many investigations have utilized a taste aversion paradigm to examine the effects of classical conditioning on an immune response. The procedure generally consists of an animal ingesting a novel flavor, and then being made ill and immunosuppressed by injection of a pharmacological agent. The animal is provided access to that flavor at a later time. The rejection of the novel flavor on the test day is called taste aversion and the depressed antibody titer has been labeled conditioned immunosuppression. The present research was designed condition a secondary immune response and expand the evaluation of such conditioning to include both antibody titer and affinity. The Enzyme Linked Immunoassay was also introduced as the procedure of choice to quantify immune reactivity. A depression in antibody titer and affinity was found following exposure to three of four test trials. Taste aversion did not correlate with the immune response as increased consumption of the novel flavor was exhibited on the third and fourth test trial. In the second experiment, the dosage of cyclophosphamide was increased. A depression in antibody affinity was found after the third and fourth test trials, which was consistent with the results of the first experiment. Unlike the first experiment, a depression in antibody titer was not attained on test days. Although taste aversion was observed in the treatment group on three of the four test trials, it had extinguished by test four. The results support the concept of conditioned suppression of an antigen specific immune response by exposure to the taste aversion paradigm. An important contribution of the present research was the use and modification of a precise and sensitive assay for quantification of titer and affinity; the demonstration of conditioned suppression in both antibody titer and affinity; and the demonstration of conditioned immunosuppression with a single component CS.

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Chou, Chiu-wen, and 周秋雯. "A study of the expression of NF-kB in central nervous system of rats with neuropathic pain." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44902542.

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Vallejo, M. "Functional interactions between amines and peptides in the central nervous system." Thesis, Brunel University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384097.

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Toledo, Izabela Martina Ramos Ribeiro de. "Ação central da insulina e do sistema nervoso autônomo sobre a produção hepática de glicose de ratos não anestesiados." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-25072012-102910/.

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A glicose é considerada o combustível mais importante para a manutenção das atividades de diversos tecidos corporais. O fígado é um órgão chave na manutenção da homeostase da glicose e para que isto ocorra é necessária a presença de hormônios, tais como a insulina que pode desempenhar sua função agindo tanto em nível periférico como centralmente. Além disso, estudos demonstram que o sistema nervoso autônomo (SNA) desempenha uma função extremamente importante no controle da glicemia. Sendo assim, o objetivo deste trabalho foi avaliar o efeito da insulina injetada no sistema nervoso central sobre a produção hepática de glicose (PHG), além de verificar o papel do SNA na modulação dessa variável em ratos livres de anestesia. Para isto, utilizamos um modelo animal de hiperatividade simpática, (SHR) e seu controle (Wistar). Antecedendo todos os experimentos, os animais foram mantidos em privação alimentar por um período de 12 h. A insulina e/ou insulina denaturada (controle-veículo) foi injetada no ventrículo lateral (VL) cerebral (100hU/ml) e a PHG, PAM e FC foram monitorados aos 2, 5, 10, 20 e 30 min. subsequentes. No grupo Wistar observamos uma queda máxima na PHG aos 10 min. após a microinjeção de insulina no VL (81,4 mg/dL) quando comparados ao seu valor basal antes da insulina (110mg/dL) e ao grupo controle (insulina denaturada) no mesmo decurso temporal (117,5 mg/dL). Em outro grupo experimental verificamos que o antagonismo periférico dos receptores muscarínicos (metil-atropina, 2mg/Kg, i.v.) foi capaz de bloquear a queda na PHG decorrente da ação central da insulina no mesmo decurso temporal (92mg/dL aos 10\' vs 88mg/dL no basal). Por outro lado, o antagonismo periférico dos receptores adrenérgicos (fentolamina, 3mg/Kg e propranolol, 0,5mg/Kg, i.v., respectivamente) não afetou a queda da PHG após administração da insulina no VL. No grupo SHR a insulina injetada no VL não promoveu alterações na PHG nos tempos avaliados. A PAM e FC não sofreram qualquer alteração após a injeção central de insulina em ambas as linhagens de animais. Para avaliar a função do SNA sobre a PHG basal independente da ação central da insulina de ambas as linhagens realizamos o antagonismo periférico dos receptores adrenérgicos e muscarínicos e a PHG foi monitorada aos 2, 5, 10, 20, 30, 40, 50 e 60 min. subsequentes. Os resultados mostraram que o bloqueio adrenérgico diminuiu a PHG com maior queda aos 40 min. tanto nos animais Wistar (79 mg/dL; -25%) quanto nos SHR (93 mg/dL; -22%) em relação ao basal (Wistar: 106 mg/dL e SHR: 118 mg/dL). O bloqueio periférico dos receptores muscarínicos não alterou a PHG em ambas as linhagens. O conjunto dos resultados obtidos nos leva a concluir que, durante uma situação de jejum prolongado, a alça parassimpática do SNA é a principal responsável pela rápida queda na PHG causada pela ação central da insulina em animais Wistar. Por outro lado, o sistema autonômo simpático desempenha maior influência tônica no controle da PHG basal do que a alça parassimpática, independente da ação central da insulina tanto em SHR quanto em Wistar.
Glucose is considered the most important fuel for the maintenance activities of the tissues. The liver is a key organ in maintaining glucose homeostasis and for this, requires the presence of hormones such as insulin that can perform its function by acting both peripherally and centrally. In addition, studies show that the autonomic nervous system (ANS) plays an extremely important role in glucose control. Therefore, the aim of this study was to evaluate the effect of insulin injected into the central nervous system on hepatic glucose production (HGP), and verifies the role of ANS in the modulation of this variable in conscious rats. For this, we used an animal model of sympathetic hyperactivity (SHR) and its control (Wistar). Preceding all experiments, the animals were kept in starvation for a period of 12 h. Insulin and / or denatured insulin (control vehicle) was injected into the lateral ventricle (LV) of the brain (100hU/ml) and HGP, MAP and HR were monitored at 2, 5, 10, 20 and 30 min. In the Wistar group we observed a maximal drop in PHG 10 min after microinjection of insulin in the VL (81.4 mg / dL) compared to baseline before insulin (110mg/dl) and the control group (insulin denatured) in the same time course (117.5 mg / dL). In another experimental group we found that antagonism of peripheral muscarinic receptors (methyl-atropine 2mg/kg, iv) was able to block the fall in HGP resulting from the action of insulin at the same time course (92mg/dL to 10\' vs 88mg / dL at baseline). On the other hand, the antagonism of peripheral adrenergic receptors (Phentolamine and propranolol 3mg/kg, 0.5 mg / kg, iv, respectively) did not affect the fall of HGP after administration of insulin in the VL. In the SHR group insulin injected into the VL did not promote changes in HGP in the times studied. The MAP and HR did not change after the central injection of insulin in both strains of animals. To evaluate the role of ANS on the baseline HGP independent of central action of insulin in both strains we performed the peripheral antagonism of adrenergic and muscarinic receptors and HGP was monitored at 2, 5, 10, 20, 30, 40, 50 and 60 min. The results showed that the adrenergic blockade reduced the HGP with a greater decrease at 40 min. both in Wistar (79 mg / dL, -25%) and in SHR (93 mg / dL, -22%) compared to baseline (Wistar: 106 mg / dL and SHR: 118 mg / dL). The blockade of peripheral muscarinic receptors did not alter the PHG in both strains. The set of results leads us to conclude that during starvation, the handle of the parasympathetic ANS is primarily responsible for the rapid drop in HGP caused by central action of insulin in Wistar. On the other hand, the autonomic sympathetic system plays a greater influence on the tonic baseline control of HGP than the parasympathetic system, independent of the central action of insulin in both SHR and Wistar.

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Sreemantula, Sai Nandini. "Glutamate Transporter 1 in the Central Nervous System: Potential Target for the Treatment of Alcohol Dependence." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1333546775.

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Letaif, Olavo Biraghi. "Avaliação do efeito do estrógeno na lesão medular experimental em ratos." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5140/tde-27082014-145453/.

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Este estudo teve como objetivo avaliar a influência do tratamento com estrógeno em ratos submetidos à lesão medular aguda experimental. A lesão foi produzida por meio de um equipamento computadorizado para impacto medular, o NYU Impactor, que promoveu a queda de um peso de altura de 12,5 mm sobre a medula do animal. Utilizamos 20 ratos Wistar que foram separados em dois grupos de 10 animais cada: Grupo 1, com ratos submetidos a lesão medular e depois a terapia com 17-beta estradiol ainda sob anestesia, o grupo experimental; Grupo 2, com ratos submetidos apenas à lesão medular, o grupo controle. Os animais foram observados por 42 dias. A recuperação funcional motora foi avaliada pela escala de Basso, Beattie e Bresnahan (BBB) nos dias 2, 7, 14, 21, 28, 35 e 42 após a lesão, e pelo exame de potencial evocado motor no dia 42. Foi também realizada avaliação histopatológica da área da lesão medular após eutanásia, no dia 42. Os resultados das avaliações da escala BBB evidenciaram que o grupo experimental apresentou melhora significativamente superior em relação ao outro grupo desde o 28o dia até o 42o dia de observação. Os resultados das avaliações por exame de potencial evocado revelaram que o grupo experimental apresentou melhora estatisticamente significante em relação ao grupo controle. Os resultados das avaliações anatomopatológicas pela histomorfometria mostraram melhor recuperação neurológica do grupo experimental com relação à proporção numérica e ao diâmetro das fibras nervosas contadas. A conclusão é que a administração de estrógeno em ratos submetidos à lesão medular mostrou benefícios na recuperação neurológica e funcional motora dos animais tratados
This study aimed to evaluate the influence of estrogen treatment in rats with experimental acute spinal cord injury. The injury was produced using a computerized device for spinal cord impact, the NYU Impactor, which promoted the injury by the falling of a weight on the animal\'s spine from a 12.5 mm-height. Twenty male Wistar rats were divided into two groups of 10 animals each: Group 1, rats with spinal cord injury and undergoing estrogen therapy with 17-beta estradiol, while still anesthetized, the experimental group; Group 2, rats that underwent spinal cord injury only, the control group. Animals were observed for 42 days. The neurological recovery was verified by assessing functional motor recovery by the scale of Basso, Beattie and Bresnahan (BBB) on the 2nd, 7th, 14th, 21st, 28th, 35th and 42nd days after injury, and by quantifying motor evoked potential in the 42nd day. Histopathological evaluation of the area of spinal cord injury was performed after euthanasia in the 42nd day. Results of the BBB scale evaluation showed that the experimental group had significantly greater improvement compared to the other group since the 28th day until the 42nd day of observation. The results of evaluations by the evoked potential test revealed that the experimental group showed statistically significant improvement compared to the control group. The results of the histomorphometry evaluations showed better neurological recovery in the experimental group with respect to the numerical proportion and diameter of nerve fibers counted. The conclusion is that the administration of estrogen in rats with spinal cord injury showed benefits in neurological and functional motor recovery of the treated animals

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19

Varriano, Ana Augusta. "Alterações clínicas e bioquímicas decorrentes do estresse crônico imprevisível e do estresse oxidativo em ratos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-17112008-094855/.

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O estudo dos efeitos do estresse em modelos animais contribui para investigar os mecanismos de sinalização envolvidos nas enfermidades humanas. O projeto foi dividido em duas partes. Primeiramente investigou-se o efeito do estresse crônico imprevisível (ECI) na evolução clínica da encefalomielite autoimune experimental (EAE) e as concentrações circulantes de corticosterona (CORT). O ECI agravou os sinais clínicos da EAE em ratos, mas as concentrações plasmáticas de CORT durante o desenvolvimento da doença pareceram depender unicamente do desafio imunológico. Posteriormente investigaram-se os mediadores inflamatórios e o estresse oxidativo em diversas áreas do SNC de ratos submetidos à isquemia e reperfusão mesentérica. Foram observadas alterações distintas, conforme o tecido analisado, na expressão gênica de NOS e COX, atividade da NOS Ca2+-dep e da arginase e no conteúdo de TBARS. Conclui-se que, nas primeiras horas de reperfusão intestinal, as estruturas analisadas reagem diferentemente ao estresse oxidativo.
The study of stress effects in different animal models help to clarify signalization mechanisms involved in human diseases. The present project was divided in two parts. Firstly, we investigated the effects of chronic unpredictable stress (CUS) on the course of experimental autoimmune encephalomyelitis (EAE) and circulating corticosterone (CORT) concentrations. CUS aggravated the clinical signs of the disease in Lewis rats. However, plasma CORT during the development of clinical signs seemed to be solely dependent on the immunological challenge. Secondly, we investigated the oxidative and defense mechanisms in several CNS regions of rats submitted to an intestinal ischemia-reperfusion model. There were distinct results, as tissue analysis, in genic expression of NOS and COX, calcium-dependent nitric oxide synthase and arginase activities and TBARs content. Based on these results, we concluded that, at least during the first two hours of intestinal reperfusion, CNS lesions may be efficiently prevented by defense mechanisms able to modulate the oxidative injury.

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20

Burton, Susan Frances. "A study of the effects of the pineal hormone, melatonin, on dopaminergic transmission in the central nervous system of rats." Thesis, Rhodes University, 1990. http://hdl.handle.net/10962/d1001463.

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Dopamine mechanisms in the central nervous system are important in the control of both normal and abnormal motor function. The recent observations in both animal and human studies, that melatonin, the principal hormone of the pineal gland, may have a role in the control of movement and the pathophysiology of movement disorders, have given rise to the concept that melatonin may have a modulatory influence on central dopaminergic neurotransmission. This study makes use of three animal behavioural models as well as a biochemical model of central dopaminergic function to further investigate the concept. Results from studies using the biochemical model, which investigated the effect of melatonin on dopamine and apomorphine stimulation of dopamine-sensitive adenylate cylase, suggest that melatonin is neither a competitive antagonist nor agonist at the D₁ receptor level, although the possibility of physiological stimulation or antagonism is not excluded. In behavioural studies, prior melatonin mg/kg administration (1 and 10 (8M) ip) inhibited apomorphine induced stereotypy and locomotor activity in normal rats, and apomorphine-induced rotational behaviour in 6-hydroxydopamine and quinolinic acid lesioned rats. The possibility that these results may have physiological significance is borne out by the observation that, under enviromental lighting conditions that are associated with raised endogeous melatonin levels, apomorphine- induced stereotypy and locomotor activity is attenuated. The general conclusion is that melatonin has an inhibitory influence on central nervous system dopaminergic function, suggesting therefore, that the pineal gland and melatonin may have a role in the pathophysiology and treatment of movement and behavioural disorders associated with dopaminergic dysfunction

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21

Coderre, Terence J. (Terence James). "Peripheral and central mechanisms of pain and hyperalgesia : effects of adrenergic and sensory neuron blockade on autotomy and pain sensitivity following injury." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72030.

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The mechanisms of pain and hyperalgesia were examined in rats following cutaneous-heat and peripheral-nerve injury. Central mechanisms of hyperalgesia were indicated since a heat injury produced a decrease in foot-withdrawal latencies in the paw contralateral to the injury and an increase in autotomy of the injured paw following section of the sciatic and saphenous nerves. The reduced contralateral foot-withdrawal latencies were reversed by spinal anesthesia and subcutaneous guanethidine, but were unaffected by local anesthetics and capsaicin at the site of injury. The enhancement of autotomy produced by an injury was reduced by spinal anesthesia and a combination of intrathecal capsaicin and subcutaneous guanethidine. Both intrathecal substance P and systemic noradrenaline produced an increase in autotomy following nerve lesions; guanethidine, but neither capsaicin nor procaine, produced a decrease in autotomy. A reduction in inflammation and hyperalgesia within an injured paw was produced by local capsaicin, but not by guanethidine. The results suggest that central mechanisms, such as spinal hyperactivity, combined with peripheral neurogenic mechanisms are involved in the production of hyperalgesia following heat injury. Pain and hyperalgesia following nerve injury are proposed to be due to spinal cord plasticity resulting from deafferentation and abnormal sympathetic activity.

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22

Ellis, Rebecca Catherine. "Characterization of cathepsin b mrna and protein expression, enzymatic activity and cellular localization following contusion spinal cord injury in rats." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007160.

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Thesis (Ph.D.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 97 pages. Includes Vita. Includes bibliographical references.

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23

Lewandowski, Thomas A. "Toxicokinetic and toxicodynamic modeling of the effects of methyl mercury on development of the embryonic rat midbrain /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8450.

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Kawashita, Priscila Tiemi. "O nucleo accumbens e a substancia cinzenta periaquedutal modulam de modo distinto a hiperalgesia inflamatoria cronica e aguda em ratos." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289268.

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Orientadores: Adriana Pelegrini da Silva, Claudia Herrera Tambeli
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: A modulação da dor pelo sistema nervoso central (SNC) consiste na inibição ou facilitação da excitabilidade do corno dorsal da coluna espinhal. O núcleo Accumbens (Nacc) e a Substância Cinzenta Periaquedutal (PAG) são duas importantes estruturas envolvidas na modulação da dor pelo SNC. A proposta deste estudo foi investigar o papel destas estruturas na modulação da hiperalgesia inflamatória aguda e persistente, induzida pela administração de Prostaglandina E2 (PGE2) na pata de ratos. A administração local subcutânea de PGE2 induz um quadro de hiperalgesia que cede completamente em 24 horas. Entretanto, duas semanas de injeções intraplantares de PGE2 induzem uma hiperalgesia que persiste por 30 dias após cessar o tratamento. Os resultados deste estudo demonstraram que a microinjeção no NAcc de lidocaína ou de cloreto de cobalto (CoCl2 ), um bloqueador de canal de Cálcio, reduziu significativamente a hiperalgesia persistente, mas não modificou a hiperalgesia mecânica aguda induzida pela PGE2 , medida tanto pelo teste de Randall-Selitto quanto pelo teste de Von Frey. Em contraste, a lidocaína ou o CoCl2 injetados na PAG não modificaram a hiperalgesia persistente, mas aumentaram a hiperalgesia aguda induzida pela PGE2 . Também demonstramos que a administração de L-Glutamato no NAcc restaurou a hiperalgesia persistente inibida pela administração local de Dipirona na pata. Estes resultados sugerem que o NAcc, mas não a PAG, está envolvido na manutenção da hiperalgesia persistente induzida pela PGE2 e pode também participar na recorrência da dor crônica de origem inflamatória
Abstract: The pain modulation by Central Nervous System (CNS) consists in inhibition or facilitation of the spinal dorsal horn excitability. The nucleus accumbens (NAcc) and periaqueductal gray matter (PAG) are two important structures involved in the pain modulation by CNS. The purpose of the present study was to investigate the role of NAcc and PAG on the modulation of the acute and persistent inflammatory hyperalgesia induced by prostaglandin E2 (PGE2) in rat. The local subcutaneous administration of PGE2 induces hiperalgesia that is completely resolved in 24 h. However, 2 weeks of daily intraplantar treatment with PGE2 induces hyperalgesia that persists for more than 30 days after the treatment cessation. The findings of this study demonstrated that the local injection of lidocaine or CoCl2, a calcium channel blocker in the NAcc significantly reduced the persistent, but did not modify acute PGE2-induced mechanical hyperalgesia, measured by either Randall-Sellito or Von Frey tests. In contrast, lidocaine or CoCl2, injected in the PAG did not modify the persistent hyperalgesia, but increased the acute hyperalgesia induced by PGE2. We also demonstrated that the administration of L-glutamate in NAcc restored the persistent hyperalgesia inhibited by the local administration of dipyrone in the hind paw. These results suggest that NAcc, but not PAG is involved in the maintenance of the PGE2-induced persistent hyperalgesia and may also be implicated in the recurrence of chronic pain of inflammatory origin
Mestrado
Fisiologia Oral
Mestre em Odontologia

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Vieira, Vinícius de Almeida. "Avaliação do comportamento de ratas Wistar tratadas durante a gravidez com Hypericum perforatum L. no período pós-natal e de seus descendentes (F1) na fase adulta." Universidade Federal de Juiz de Fora, 2012. https://repositorio.ufjf.br/jspui/handle/ufjf/1562.

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FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
A depressão gestacional é um assunto de grande preocupação, considerando-se os riscos de reincidência de sintomas futuros e os efeitos deletérios à saúde materna e de seus descendentes. Os antidepressivos sintéticos não diminuem a reincidência de sintomas no pós-parto, possuem muitos efeitos colaterais e não são isentos de riscos ao feto. O Hypericum perforatum L. (HP) é um fitofármaco muito utilizado no tratamento da depressão, que apresenta menos efeitos colaterais, parece não apresentar efeitos teratogênicos, e o seu uso demonstrou diminuição da recorrência futura de sintomas. Por outro lado, ainda não se sabe seus reais efeitos, quando utilizado na gravidez, no comportamento futuro da mãe e no desenvolvimento comportamental de sua prole. Portanto, este trabalho avaliou o comportamento de ratas tratadas durante a gravidez com HP no período pós-natal e de seus descendentes na fase adulta. Ratas prenhas foram divididas em três grupos tratados (T1, T2 e T3) e um grupo controle (C), que receberam, por via intragástrica e uma vez ao dia durante toda a gestação, o extrato de HP nas doses de 36, 72 e 144 mg/kg e água destilada, respectivamente. As ratas foram submetidas, com 10 e 60 dias de pós-natal, ao teste do labirinto em cruz elevado para avaliação da ansiedade e aos testes do nado forçado e suspensão da cauda para avaliação da depressão. Os seus filhotes machos foram divididos em quatro grupos, de acordo com o tratamento recebido pelas mães, e avaliados aos 90 dias de vida. Eles foram submetidos aos testes da barra giratória e do tempo de sono induzido por barbitúricos para avaliação de uma possível ação no sistema nervoso central (SNC), aos testes do labirinto em cruz elevado e da placa perfurada para avaliação da ansiedade, e aos testes do nado forçado e de suspensão da cauda para avaliação da depressão. As ratas pertencentes aos grupos T2 e T3, apresentaram um menor comportamento ansioso no teste do labirinto em cruz elevado, e um menor comportamento depressivo nos testes de suspensão da cauda e nado forçado, quando avaliadas 10 e 60 dias após o nascimento dos filhotes e suspensão do tratamento. Nos testes da barra 8 giratória e do tempo de sono induzido por barbitúricos, os descendentes das ratas dos grupos T2 e T3 apresentaram um desempenho sugestivo de ação do HP no SNC, quando comparados aos descendentes das ratas do grupo controle. Nos testes da placa perfurada e do labirinto em cruz elevado e nos testes de suspensão da cauda e do nado forçado, os animais destes mesmos grupos apresentaram um comportamento menos ansioso e depressivo, respectivamente. Portanto, o uso de HP na gestação diminuiu o comportamento depressivo e de ansiedade de ratas Wistar no período pós-natal e também de seus descendentes (F1) quando alcançam a fase adulta.
Gestational depression is a subject of great concern, considering the risks for the recurrence of symptoms and its harmful effects to the mother's and offspring's health. Synthetic antidepressants do not decrease the recurrence of symptoms in the postpartum period, present many side effects, and are not exempt of risks to the fetus. Hypericum perforatum (HP) is a phytopharmacon largely used in the treatment of depression, presents less side effects, does not seem to present teratogenic effects, and its use showed a decrease in the future recurrence of symptoms. On the other hand, its real effects in the future behavior of the mother and in the behavioral development of her offspring when used during pregnancy is not yet known. Therefore, this study evaluated the behavior of rats treated with HP during pregnancy in the postnatal period and of their offspring in their adult phase. Pregnant rats were divided into three treated groups (T1, T2 and T3) and a control group (C) that received, intragastrically, once a day, during the gestational period, HP extract in doses of 36, 72 and 144 mg/kg respectively and distilled water. At ten and 60 days of postnatal life, the rats were submitted to the elevated cross maze test for evaluation of anxiety and to the forced swim and tail suspension tests for evaluation of depression. Their male offspring were divided into four groups, according to the treatment received by the mothers, and evaluated at 90 days of age. They were submitted to the rotarod and barbiturate sleep-induced tests for evaluation of a possible action on the central nervous system (CNS), to the elevated cross maze and hole-board tests for evaluation of anxiety, and to the forced swim and tail suspension tests for evaluation of depression. The rats from groups T2 and T3 displayed less anxious behavior in the elevated cross maze test, and less depressive behavior in the tail suspension and forced swim tests when evaluated 10 and 60 days after the parturition of their offspring and discontinuation of treatment. In the rotarod and barbiturate sleep-induced tests, the offspring of the rats from groups T2 and T3 presented a suggestive performance of the HP action in the CNS, when compared with the offspring of 10 the rats from the control group. In the hole-board and elevated cross maze tests, as well as in the tail suspension and forced swim tests, the animals of these groups displayed less anxious and depressive behavior, respectively. Therefore, the use of HP during pregnancy reduced the depressive and anxiety behavior in Wistar rats in the postnatal period and also in their offspring (F1) when they reached their adult phase.

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26

Sherman, John Mark. "The GABAa receptor in the central nervous system of a rat model of epilepsy." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc798322/.

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27

Vendrame, Rafaela Fadoni Alponti. "Aminopeptidase neutra, dipeptidil peptidase IV, CD13, CD26 e Fos no hipotálamo e hipocampo de ratos com obesidade induzida por glutamato monossódico e privados de alimento." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-20032009-122119/.

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Alterações na atividade de peptidases no sistema nervoso central (SNC) de adictos a narcóticos, abstinentes dependentes de opióides, diabéticos e indivíduos com desequilíbrio hidrosalino, têm sido achados instigantes no contexto atual dos conhecimentos sobre o balanço energético. Neste sentido, são particularmente interessantes o fenômeno da proteólise irrestrita e o envolvimento de diversos peptídeos do SNC, especialmente no hipotálamo e hipocampo, como as incretinas, neuropeptídeo Y, peptídeo YY, peptídeos derivados da proopiomelanocortina (melanocortinas e beta-endorfinas), somatostatina, vasopressina e angiotensinas. O presente estudo avaliou a hipótese de que aminopeptidases que têm alguns desses peptídeos como substratos, a aminopeptidase neutra (APN) (sensível PSA, e insensível APM/CD13, à puromicina) e a dipeptidil peptidase IV (DPPIV/CD26) (sensível - DPPIV-DS, e insensível - DPPIV-DI à diprotina), poderiam relacionar-se com a obesidade induzida por glutamato monossódico (MSG) e com o estado de privação alimentar. Foram analisadas as expressões gênica e protéica da CD13 e CD26, as atividades enzimáticas de PSA, APM, DPPIV-DS e DPPIV-DI em fração solúvel e de membrana solubilizada, a ativação celular (imuno-reatividade a Fos), a distribuição imuno-histoquímica regional de CD13 e CD26 no hipotálamo e hipocampo e as correlações entre atividades peptidásicas, massa corporal, índice de Lee, massa dos depósitos de gordura periepididimal e retroperitoneal, comprimento naso-anal e glicemia de ratos obesos MSG e normais, sob regime de privação ou alimentação normal. Comparativamente aos controles, os animais MSG apresentaram: (i) aumento da massa absoluta de gordura retroperitoneal, índice de Lee, expressão protéica CD13 membranal do hipocampo, expressão protéica policlonal CD26 membranal do hipotálamo, atividade DPPIV-DI e expressão protéica monoclonal CD26 membranal do hipocampo; e (ii) diminuição da massa corporal absoluta, comprimento nasoanal, expressão gênica de CD13, expressão protéica membranal de CD13, expressão protéica policlonal de CD26 solúvel e membranal, atividades PSA solúvel e DPPIV-DI solúvel e membranal hipotalâmicas e DPPIV-DS membranal do hipocampo. A privação de alimento também influencia alguns destes parâmetros. As correlações entre os parâmetros biométricos confirmaram características deste modelo de obesidade e adicionalmente sugeriram que a deficiência e a sobrecarga relativas de captação de glicose, respectivamente pela gordura periepididimal e retroperitoneal, poderiam estar associadas ao desenvolvimento do diabetes melito tipo 2 no obeso MSG. Confirmou-se a identidade da proteína CD13 com a atividade peptidásica APM. A DPPIV-DI foi identificada como a CD26 canônica. Em geral, o presente estudo evidenciou o envolvimento das atividades PSA, DPPIV-DI e -DS hipotalâmicas (mas não da APM) e das proteínas CD13 e CD26, na regulação endócrina do balanço energético (provavelmente via atuação sobre neuropeptídeo Y, somatostatina e opióides). No hipocampo, o padrão destas alterações foi compatível com efeito deletério sobre memória, aprendizado (PSA e APM) e comportamento emocional (DPPIV-DI e DS). CD13 e CD26 apresentaram ampla distribuição no hipotálamo, a qual, em condições normais, foi coincidente com a imuno-reatividade à Fos nos núcleos supraóptico, periventricular, retroquiasmático e arqueado. Nestas áreas, relacionadas ao controle do balanço energético, ocorreram alterações densitométricas da imuno-reatividade a CD13, CD26 e Fos em função da obesidade MSG e/ou da privação de alimento. Em suma, proteínas com atividades de aminopeptidase neutra 9 ou dipeptidil peptidásica do tipo IV e/ou homólogas à CD13 ou CD26 são fatores fisiopatológicos e alvos farmacológicos potenciais de distúrbios do metabolismo energético.
Alterations of peptidase activity levels in the central nervous system (CNS) in drug addicts, abstinent opioid-dependent, diabetic and subjects with disrupted hydrosaline equilibrium, have been arousing findings in the context of current knowledge about regulatory mechanisms of food intake and energy balance. In this sense, the involvement of leptin, ghrelin, insulin and other peptides in the CNS, including incretins, neuropeptide Y, peptide YY, proopiomelanocortins (melanocortins and _-endorphin), somatostatin and vasopressin, which are susceptible to hydrolysis by aminopeptidases (APs), mainly in the hypothalamus and hippocampus, are particularly interesting. The present work evaluated if aminopeptidase activities involved in the hydrolysis of these peptides, i.e. neutral AP (APN) (sensitive- or insensitive-puromycin AP, PSA or APM/CD13, respectively) and dipeptidyl peptidase IV (DPPIV/CD26) (sensitive- or insensitive-diprotin dipeptidyl peptidase, DPPIV-DS or DPPIVDI, respectively), are associated with monosodium glutamate (MSG) induced obesity and food deprivation. It was analysed the gene and protein expressions of CD13 and CD26, catalytic activities of PSA, APM, DPPIV-DS and DPPIV-DI in soluble and membrane-bound fractions, cellular activation (Fos immunoreactivity) and regional immunohistochemistry distribution of CD13 and CD26, in hypothalamus and hippocampus, and inter-relations among these peptidase activities, body mass, Lee index, mass of epidydimal and retroperitoneal fat pad, naso-anal length and glycemia in normal and obese MSG rats under normal or deprived feeding regimens. Relative to control, MSG presented: (i) increased retroperitoneal mass, Lee index, CD13 protein expression in membrane-bound fraction of hippocampus, CD26 polyclonal protein expression in membrane-bound fraction of hypothalamus, DPPIV-DI activity and CD26 monoclonal protein expression in membranebound fraction of hippocampus; and (ii) reduction of body mass, naso-anal length, CD13 gene expression, CD13 protein expression in membrane-bound fraction, CD26 polyclonal protein expression in soluble and membrane-bound fraction, PSA activity in soluble fraction and DPPIV-DI activity in soluble and membrane-bound fractions of hypothalamus, and DPPIVDS in membrane-bound fraction of hippocampus. Food deprivation also influenced some of these parameters. The correlations between biometric parameters confirmed the characteristics of this obesity model and further suggested that disability and overload on the uptake of glucose, respectively by the epididymal and retroperitoneal fat, could be linked to the development of diabetes mellitus type 2 in obese MSG. CD13 protein identity with APM peptidase activity was confirmed. DPPIV-DI was identified as the canonical CD26 protein. In general, the present work revealed the involvement of PSA, DPPIV-DI and DS hypothalamic activities (but not the APM) and the CD13 and CD26 proteins, in endocrine regulation of energy balance (probably through action on neuropeptide Y, somatostatin and opioids). In the hippocampus, the patterns of these changes were consistent with deleterious effects on memory, learning (PSA and APM) and emotional behavior (DPPIV-DI and DS). CD13 and CD26 presented wide distribution in hypothalamus, which, in normal conditions, is coincident with Fos immunoreactivity in the supraoptic, periventricular, retrochiasmatic and arcuate nuclei. In these areas, related to the control of energy balance, densitometric changes of CD13, CD26 and Fos immunoreactivity occurred according to the obesity MSG and/or food deprivation. Briefly, proteins presenting neutral aminopeptidase or dipeptidyl peptidase IV 11 activities and/or CD13 or CD26 homologous are physiopathological factors and potential pharmacological targets of energetic metabolism disturbances.

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28

易亮華 and Leung-wah Yick. "Promotion of neuronal survival and axonal regeneration in Clarke's nucleus after spinal cord injury in adult rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31239651.

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29

Melloni, Richard H. "Dynamics of Neuron-Specific Gene Expression During Development and in Response to Selective Lesions of the Rat Central Nervous System: A Dissertation." eScholarship@UMMS, 1993. https://escholarship.umassmed.edu/gsbs_diss/204.

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Synapse development and injury-induced reorganization in the nervous system have been extensively characterized morphologically, although, relatively little is known regarding the molecular and biochemical events that underlie these processes. In an attempt to better understand, at the molecular level, the role of the expression of synaptic proteins during synapse establishment and regeneration, this dissertation examines the dynamics of expression of the neuron-specific gene synapsin I during development and in response to selective lesions of the rat central nervous system. Synapsin I is the best characterized member of a family of nerve-terminal specific phosphoproteins implicated in the regulation of neurotransmitter release. During development, the expression of synapsin I correlates temporally and topographically with synapse formation, and recent physiological studies by Lu et al., (1992) have suggested that synapsin I may participate in the functional maturation of synapses. To better understand the temporal relationship between synapsin I gene expression and particular cellular events during development, we have used in situhybridization histochemistry to localize synapsin I mRNA in the rat central and peripheral nervous systems throughout embryonic and postnatal development, and into the adult period. During development, from the earliest embryonic time point examined (E12), the expression of the synapsin I gene was detectable in both the rat central and peripheral nervous systems. While, in general, levels of synapsin I mRNAs were high in utero, synapsin I cDNA probes revealed specific patterns of hybridization in different regions of the embryonic nervous system. To precisely determine the temporal onset of expression of the synapsin I gene during neuronal development, we examined in detail the appearance of synapsin I mRNA during the well characterized postnatal development of the cerebellum and hippocampus. In both regions, the onset of synapsin I gene expression correlated with the period of stem cell commitment to terminal differentiation. In a second phase, in accord with prior analyses, synapsin I gene expression increases to a maximum for a given neuronal population during synapse formation. In the adult rat brain, our data demonstrates a widespread yet regionally variable pattern of expression of synapsin I mRNA similar to that seen at earlier time points, with noteworthy exceptions. The greatest abundance of synapsin I mRNA was found in the pyramidal neurons of the CA3 and CA4 fields of the hippocampus, and in the mitral and internal granular cell layers of the olfactory bulb. Other areas abundant in synapsin I mRNA were the layer n neurons of the piriform and entorhinal cortices, the granule cell neurons of the dentate gyrus, the pyramidal neurons of hippocampal fields CA1 and CA2, and the cells of the parasubiculum. In general, the pattern of expression of synapsin I mRNA paralleled those encoding other synaptic terminal-specific proteins, such as synaptophysin, VAMP-2, and SNAP-25. Then, to determine specifically how synapsin I mRNA levels are related to levels of synapsin I protein in the adult rat brain, we employed in situhybridization histochemistry and immunohistochemistry to examine in detail the local distribution of both synapsin I mRNA and protein in the hippocampus. In short, these data revealed differential levels of expression of synapsin I mRNA and protein within defined synaptic circuits of the rat hippocampus. Based on these data we hypothesized that locally high levels of synapsin I mRNA in neuronal somata may reflect the ability of the nervous system to respond to select enviromental stimuli and/or injury by producing longterm changes in synaptic circuitry. To test this hypothesis and to better understand the regulation and putative role of synapsin I gene expression in the development of functional synapses in the central nervous system, we first examined the developmental pattern of expression of the synapsin I gene; in dentate granule neurons of the dentate gyrus and their accompaning mossy fibers during the main period of synaptogenic differentiation in the rat hippocampus. The results of these studies indicate a significant difference between the temporal expression of synapsin I mRNA in dentate granule cell somata and the appearence of protein in their mossy fiber terminals during the posmatal development of these neurons. Next, to investigate the regulation and putative role of synapsin I gene expression during the restoration of synaptic contacts in the central nervous system, we examined the expression of the synapsin I mRNA and protein following lesions of hippocampal circuitry. These studies show marked changes in the pattern and intensity of synapsin I immunoreactivity in the dendritic fields of dentate granule cell neurons following perforant pathway transection. In contrast, changes in synapsin I mRNA expression in target neurons, and in those neurons responsible for the reinnervation of this region of the hippocampus, were not found to accompany new synapse formation. On a molecular level, both developmental and lesion data suggest that the expression of the synapsin I gene is tightly regulated in the central nervous system, and that considerable changes in synapsin I protein may occur in neurons without concommitant changes in the levels of its mRNA. From a functional standpoint, our results suggest that the appearance of detectable levels of synapsin I protein in developing and sprouting synapses does not reflect simply synaptogenesis, but coincides with the acquisition of function by those central synapses.

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Rodella, Patricia. "Efeitos da administração de taurina na função cardiovascular e na neurogênese hipocampal de ratos submetidos ao consumo induzido de etanol /." Araraquara, 2016. http://hdl.handle.net/11449/151134.

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Orientador: Man Chin Chung
Coorientador: Carlos Cesar Crestani
Banca: Silvia Honda Takada
Banca: Ellen Cristini de Freitas
Banca: Priscila Longhin Bosquesi de Oliveira
Banca: Eduardo Rene Perez Gonzales
Resumo: O consumo excessivo de etanol está relacionado a diminuição da neurogênese hipocampal e a diversas patologias cardiovasculares, como a hipertensão. A taurina é um aminoácido não-essencial encontrado principalmente em estruturas cujos tecidos são mais excitáveis, como músculo esquelético, tecido cardíaco, vasos sanguíneos e sistema nervoso central. Níveis normais deste nutriente são essenciais para o correto funcionamento do organismo e sua depleção pode precipitar diversos quadros patológicos. A taurina tem apresentado resultados promissores tanto no sistema cardiovascular quanto no sistema nervoso central. Desta maneira, o objetivo deste trabalho foi estudar os efeitos da taurina na função cardiovascular bem como na neurogênese hipocampal de ratos submetidos ao modelo de consumo forçado de etanol. Dessa forma, ratos Wistar de aproximadamente 250 gramas receberam soluções crescentes de etanol (5% na primeira semana, 10% na segunda semana e 20% na terceira e quarta semana), sem a oferta de água; o grupo controle recebeu apenas água. A taurina foi administrada (i.p., 300 mg/kg) diariamente durante 28 dias e os animais do grupo controle receberam injeção apenas do veículo. O presente trabalho foi dividido em dois experimentos. No primeiro, a taurina foi administrada juntamente com a oferta de etanol. Já o segundo experimento, os animais foram expostos ao etanol e depois, receberam a taurina. Os resultados do Experimento 1 não mostraram alterações significativas na função cardiov... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Excessive ethanol consumption is related with decrease in hippocampal neurogenesis and various cardiovascular disorders such as hypertension. Taurine is a non-essential amino acid and is found primarily in structures which are more excitable tissues, such as skeletal muscle, heart tissue, blood vessels and central nervous system. Normal levels of this compound are essential for the correct functioning of the body and its depletion may precipitate various pathological conditions. Among the various compounds studied to reverse or protect against the effects of ethanol, taurine have shown promising results both in the cardiovascular system and the central nervous system. Thus, the objectives of this study was to investigate the effects of taurine on cardiovascular function and hippocampal neurogenesis in rats submitted to the model of forced consumption of ethanol. Wistar rats of 250g of body weight received ethanol solution (5% in the first week, 10% in the second week and 20% in the third and fourth week) without the offer of water. Taurine was administered (i.p., 300 mg / kg) daily for 28 days. This study was divided into two experiments. In the first one, to analyze the protective effects of taurine on the cardiovascular system and hippocampal neurogenesis against the effects of ethanol consumption, taurine was administered along with the ethanol consumption model. In the second experiment, to analyze the effects of taurine in reversing the effects of ethanol consumption, the animals were exposed to the ethanol consumption model and then received taurine. The results of Experiment 1 showed no significant changes in cardiovascular function... (Complete abstract click electronic access below)
Doutor

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31

Filho, Paulo Roberto Maciel. "Estudo da expressão do gene SAH e do gene codificador da proteína ATRAP em áreas do sistema nervoso central e sua relação com a gênese da hipertensão essencial verificada em ratos SHR." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-08122010-165155/.

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A hipertensão essencial é uma doença que afeta cerca de 20% da população adulta, chegando a 50% no caso dos idosos, sendo que os mecanismos de sua gênese ainda não são totalmente conhecidos. O objetivo deste trabalho é investigar a expressão de dois genes relacionados aos mecanismos renais de controle da pressão arterial em três áreas do sistema nervoso central de ratos (bulbo dorsal, bulbo ventrolateral e hipotálamo) através da técnica de PCR em tempo real, avaliando, desta forma seu possível envolvimento nos mecanismos centrais relacionados à gênese da hipertensão em ratos espontaneamente hipertensos. Um deles, o gene SAH, cujo papel ainda não foi totalmente caracterizado, tem apresentado taxas de transcrição mais altas em ratos espontaneamente hipertensos (SHR) em relação aos correspondentes normotensos WKY. O segundo gene, codificador da proteína associada ao receptor AT1 da angiotensina II (ATRAP) está relacionado com a internalização destes receptores, tendo, portanto, uma grande importância nos mecanismos reguladores da pressão arterial. Nossos resultados mostram, pela primeira vez, a transcrição de ambos os genes nas três áreas do sistema nervoso relacionadas com o controle central da pressão arterial. Ainda não foi possível estabelecer uma relação entre a expressão do gene SAH com o desenvolvimento da hipertensão em qualquer dos estágios do desenvolvimento da linhagem SHR. O gene codificador da proteína ATRAP apresentou um aumento de expressão nos ratos hipertensos entre 1 e 2 meses de idade, período importante na gênese da hipertensão nesta cepa. Desta forma, este estudo demonstra a expressão de dois genes caracterizados previamente nos rins em áreas importantes para a regulação central da pressão arterial em diferentes períodos de desenvolvimento de ratos SHR e WKY.
Essential hypertension is a disease that affects nearly 20% of the adult population, reaching 50% of the elder, and the mechanisms of its genesis are not yet completely know. This work aim to investigate two genes related to the renal mechanisms of blood pressure in three areas of central nervous system (dorsal bulb, ventrolateral bulb and hypothalamus) by means of real time PCR, in order to valuate their possible involvement in the central mechanisms of blood pressure control. One of them is the SAH gene, whose role remains to be clarified. It has higher transcription rates in hypertensive rats (SHR) than in the correspondent normotensives WKY. The other gene codifies the angiotensin II type 1 receptor associated protein (ATRAP) inducing its internalization. Thus, besides the transcriptional differences of the ATRAP protein between SHR and WKY rats, the ATRAP codifying gene is linked to blood pressure control played by means rennin-angiotensin system through AT1 receptors. Our results provide evidence for the first time, on the expression of both genes in areas of the nervous system involved with the central blood pressure regulation. It was not possible to establish a relationship between the SAH gene expression and the development of hypertension in the SHR rat. The expression of the ATRAP codifying gene was increased in the SHR between 1 and 2 months of age, which is an important period for hypertension development in this strain. Thus, this study shows the expression of SAH gene and ATRAP codifying gene in areas of nervous system of SHR and WKY important for the central regulation of blood pressure.

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Barros, Alderico Girão Campos de. "Avaliação do efeito da interleucina-6 e da eritropoetina na lesão medular em ratos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5140/tde-15032018-093626/.

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Introdução: Este estudo teve como objetivo avaliar o efeito da interleucina 6 (IL-6) e eritropoetina (EPO) na lesão medular aguda experimental em ratos. Materiais e Métodos: A lesão foi induzida pelo equipamento padronizado NYU Impactor, com queda de um peso de 10 g à distância de 12,5 mm de altura. Foram utilizados 50 ratos da linhagem Wistar, divididos em cinco grupos de 10 animais. O grupo EPO, ratos tratados com EPO; grupo EPO/IL-6, animais tratados com EPO e IL-6; grupo IL-6, administração de IL-6; grupo placebo, solução placebo; grupo Sham, procedimento sham (apenas laminectomia, sem lesão medular). Todas as drogas e soro fisiológico foram administrados por via intraperitoneal, durante três semanas. Os animais foram acompanhados por 42 dias. A recuperação motora funcional foi monitorada pela escala de Basso, Beattie e Bresnahan (BBB) nos dias 2, 7, 14, 21, 28, 35 e 42. Exame de potencial evocado foi efetuado no 42o dia, sendo realizada análise histológica qualitativa e quantitativa após eutanásia. Resultados: Os resultados das avaliações da escala BBB mostraram recuperação funcional motora superior no grupo que recebeu EPO. A administração de IL-6 isolada não mostrou benefícios em relação ao grupo que recebeu solução placebo e a associação de IL-6 com EPO mostrou resultados inferiores ao grupo que recebeu apenas EPO. Conclusão: Concluímos que uso EPO após lesão medular contusa em ratos mostrou benefícios na recuperação motora. A associação de EPO e IL- 6 mostrou benefícios, porém com resultados inferiores aos da EPO isolada. O uso isolado de IL-6 não mostrou benefícios após lesão medular contusa experimental em ratos
Introduction: The aim of this study was to evaluate the effect of interleukin-6 (IL-6) and erythropoietin (EPO) in experimental acute spinal cord injury in rats. Methods: The injury was induced by a standardized equipment for spinal cord contusion injury, the NYU Impactor, which produced the lesion by means of a 10g weight drop on the animals\' spinal cord from a 12.5-mm height. Fifty Wistar rats were divided in five groups of ten animals: Group 1 rats treated with EPO; Group 2 animals treated with EPO and IL-6; Group 3, IL-6 administration; Group 4, placebo solution; Group 5, sham procedure (only laminectomy, without spinal cord injury). All drugs and placebo solution were administered intraperitoneally for three weeks. The animals were followed up for 42 days. The functional motor recovery was monitored by the scale of Basso, Beattie and Bresnahan (BBB) on days 2, 7, 14, 21, 28, 35 and 42. Evoked potential tests were performed on the 42nd day. Qualitative and quantitative histological analysis were performed after euthanasia. Results: The group receiving EPO demonstrated superior functional motor results in the BBB scale. IL-6 administration alone did not show benefits over the placebo group solution and the IL-6 combination with EPO showed results lower than those seen in the group that received only EPO. Conclusion: We conclude that using EPO after acute spinal cord injury in rats showed benefits in motor recovery. The association of EPO and IL-6 showed benefits, but with inferior results to the isolated EPO. Isolated use of IL-6 showed no benefit after experimental spinal cord injury in rats

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Osburn, James Roy. "Importance of the kappa opoid system for ultrasonic vocalizations of young rats: Role of peripherally-versus centrally-located kappa opioid receptors." CSUSB ScholarWorks, 2008. https://scholarworks.lib.csusb.edu/etd-project/3378.

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Sonne, James H. "EFFECTS OF INTRANASALLY ADMINISTERED DNSP-11 ON THE CENTRAL DOPAMINE SYSTEM OF NORMAL AND PARKINSONIAN FISCHER 344 RATS." UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/5.

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Due to the blood-brain barrier, delivery of many drugs to the brain has required intracranial surgery which is prone to complication. Here we show that Dopamine Neuron Stimulating Peptide 11 (DNSP-11), following non-invasive intranasal administration, protects dopaminergic neurons from a lesion model of Parkinson’s disease in the rat. A significant and dose-dependent increase in an index of dopamine turnover (the ratio of DOPAC to dopamine) was observed in the striatum of normal young adult Fischer 344 rats by whole-tissue neurochemistry compared to vehicle administered controls. Among animals challenged with a moderate, unilateral 6-hydroxy-dopamine (6-OHDA) lesion of the substantia nigra, those treated repeatedly with intranasally administered DNSP-11 exhibited greater numbers of tyrosine hydroxylase (TH) positive dopaminergic neuronal cell bodies in the substantia nigra and greater TH+ fiber density in the striatum when compared to animals treated intranasally with vehicle only or a scrambled version of the DNSP-11 sequence. Lesioned animals that received intranasal DNSP-11 treatment did not exhibit abnormal, apomorphine-induced rotation behavior, contrasted with animals that received only vehicle or scrambled peptide that did exhibit significantly greater rotation behavior. In addition, the endogenous expression of DNSP-11 from the pro-region of GDNF was investigated by immunohistochemistry with a custom, polyclonal antibody. Signal from the DNSP-11 antibody was found to be differentially localized from the mature GDNF protein both spatially and temporally. While DNSP-11-like immunoreactivity extensively colocalizes with GDNF immunoreactivity at post-natal day 10, the day of maximal GDNF expression, DNSP-11-like signal was found to be present in the 3 month old rat brain with signal in the substantia nigra, ventral thalamic nucleus, dentate gyrus of the hippocampus, with the strongest signal observed in the locus ceruleus where GDNF is not expressed. Results from immunoprecipitation of brain homogenate were not consistent with the synthetic, amidated 11 amino-acid rat DNSP-11 sequence. However, binding patterns in the literature of NPY, the only homologous sequence present in the CNS, do not recapitulate the immunoreactive patterns observed for the DNSP-11 signal. This study provides evidence for a potential easy-to-administer intranasal therapeutic using the DNSP-11 peptide for protection from a 6-OHDA lesion rat model of Parkinson’s disease.

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Malta, Marília Brinati. "Efeitos adaptativos induzidos pelo estresse crônico imprevisível nos receptores do fator liberador de corticotrofina tipo 2 e de glicocorticóides no sistema nervoso central de ratos." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-13112012-120030/.

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O estresse é um fenômeno conservado e observado evolutivamente, que tem como objetivo assegurar a sobrevivência do indivíduo. Porém quando o organismo perde a capacidade de se autorregular, torna-se uma ameaça. Algumas psicopatologias, como ansiedade e depressão, sugerem o envolvimento dos sistemas CRF e noradrenérgico e de níveis elevados de GCs. Avaliamos nesse trabalho algumas alterações morfofisiológicas e comportamentais decorrentes da exposição do estresse crônico imprevisível (EI) em ratos machos. Avaliados 24 h após o último estímulo estressor, os animais submetidos ao EI apresentaram níveis elevados de corticosterona plasmática, de RNAm de CRF2 e expressão de GR em regiões encefálicas (LSi e VmH e LSi, CeA, BST e PVH, respectivamente). Essas alterações morfofisiológicas foram, em parte, decorrentes da ação de GCs e de NE. Não foram observadas alterações comportamentais quanto à anedonia e ansiedade. Dessa maneira, podemos dizer que o EI utilizado nesse estudo, foi capaz de induzir algumas alterações morfofisiológicas, porém não comportamentais.
While acute stress initiates neuronal responses that prepare an organism to adapt to challenges, chronic stress may lead to maladaptative responses that could result in diseases. Evidence suggests the involvement of CRF system and high corticosterone levels in stress-related psychiatric disorders such as anxiety and major depressive disorders. The aim of this work was to investigate whether chronic unpredictable stress (CUS) could modulate de CRF system, GR expression in the CNS and behavior in male rats. Results showed an increase in corticosterone plasmatic levels, CRF2 mRNA and GR expression in specific regions of the CNS (LSi e VmH e LSi, CeA, BST e PVH, respectively), associated with the limbic system at 24 h after the last stress session. The chronic treatment with an inhibitor of GCs synthesis (metyrapone) and adrenergic receptor antagonists (atenolol and phentolamine) prevented the CUS effects in CRF2 mRNA levels and GR expression. No anxiety or depression-like behavior was observed in rats submitted to CUS. We conclude that CUS cause biochemical alterations since the increase CRF2 mRNA levels and GR expression in limbic region, but these changes were not able to cause behavioral changes.

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Magalhães, Julia Zaccarelli. "Exposição prolongada de ratos a vareniclina: avaliação comportamental, níveis de neurotransmissores cerebrais e estudo bioquímico e anatomopatológico." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-20032017-141445/.

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A vareniclina é uma substância química sintética utilizada para o tratamento de tabagismo; atua como agonista de receptores colinérgicos nicotínicos, em especial, como agonista parcial em receptores α4β2 e α3β4, e como agonista total do receptor α7. Levando em consideração que há uma tendência de ampliação do uso clínico da vareniclina para o tratamento da dependência à diversas substâncias de padrão abusivo e que há poucos estudos relacionados aos seus efeitos sobre o comportamento, cognição e sistema motor, tornam-se necessários mais estudos sobre essa substância. Assim, no presente trabalho foram estudados os efeitos da exposição prolongada (28 30 dias) de ratos à vareniclina, avaliando-se o consumo de água e de ração, o ganho de peso e o comportamento animal, por meio dos testes de campo aberto, labirinto em cruz elevado, interação social, comportamento estereotipado, labirinto de Barnes e esquiva passiva. Ainda foram feitas as avaliações dos níveis de neurotransmissores e seus metabólitos em diferentes estruturas cerebrais, bem como avaliações hematológicas, bioquímicas séricas, urinárias e estudos anatomopatológicos e histopatológicos. Foram utilizadas três doses de vareniclina: 0,03 (dose terapêutica para o ser humano), 0,1 e 0,3 mg/kg, por via oral (gavagem). Os resultados mostraram que a exposição prolongada de ratos à diferentes doses de vareniclina não provocou toxicidade, uma vez que não houve alteração no consumo médio de água e de ração e no ganho de peso avaliados semanalmente. Quanto às avaliações comportamentais, observou-se leve aumento da atividade geral no campo aberto, bem como diminuição do tempo de interação social, não sendo capaz de alterar parâmetros neuroquímicos, hematológicos, bioquímicos séricos, urinários, anatomopatológicos e histopatológicos de ratos expostos à vareniclina.
Varenicline is a synthetic chemical used for the smoking addiction treatment; it acts as an agonist of nicotinic cholinergic receptors, in particular, as a partial agonist of receptors α4β2 and α3β4 and as a full agonist of the α7 receptor. More studies about this substance are necessary, given that its clinical use is increasingly being applied to the treatment of addiction to a variety of abusive drugs. Moreover, there are few studies on vareniciline effects on behavior, cognition and the motor system. Thus, in this study the effects of prolonged (28-30 days) exposure of rats to varenicline were evaluated. It was analyzed the water and food consumption, the weight gain and the animal behavior, through open field, elevated plus maze, social interaction, stereotyped behavior, Barnes maze and passive avoidance tests. The neurotransmitter levels and their metabolites in different brain structures were measured and hematological, serum biochemistry, urinary evaluations and pathological and histological studies were carried out. We used three doses of varenicline: 0.03 (therapeutic dose for humans), 0.1 and 0.3 mg/kg orally (gavage). The results showed that prolonged exposure of rats to different doses of varenicline did not cause toxicity, since there were no changes in average weekly consumption of water or food nor body weight gain, which were measured weekly. As for behavioral assessments, there was a slight increase in overall activity in the open field as well as decreased time of social interaction. Varenicline was not able to change neurochemical, hematological, serum biochemical, urinary, pathology and histopathology parameters of rats.

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Nascimento, Alessandro. "Effets de l'inhibition du système sympathique central sur les paramètres métaboliques et microcirculatoires chez les rats obèses avec syndrome métabolique." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ120/document.

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Les facteurs de risque cardiovasculaires et métaboliques qui caractérisent le syndrome métabolique (SM), y compris l'hypertension, l'obésité et l'intolérance au glucose, sont accompagnés d'hyperactivité sympathique. Dans cette étude, nous avons étudié les effets d'un traitement antihypertenseur chronique utilisant des médicaments d’action centrale sur les paramètres métaboliques et microvasculaires chez les rats soumis à un régime riche en gras et en sel. Pour cela, cinquante rats Wistar ont reçu un régime normal ou riche en gras pendant 20 semaines. Le groupe HFD a reçu clonidine par voie orale, rilmenidine, LNP 599 ou véhicule. La microcirculation fonctionnelle a été évaluée par vidéomicroscopie intravitale. La microcirculation structurale a été étudiée par analyse histochimique. Nous avons conclu que la modulation de l'activité sympathique corrige la raréfaction capillaire dans le muscle squelettique et le ventricule gauche dans un modèle expérimental de SM chez le rat
Cardiovascular and metabolic risk factors that characterize the metabolic syndrome (MS), including high blood pressure, obesity and glucose intolerance, are accompanied by sympathetic hyperactivity. In this study, we investigated the effects of a chronic oral antihypertensive treatment using centrally-acting sympatho-inhibitory drugs on the metabolic and microvascular parameters in rats under long-term high-fat diet with salt supplementation. For that, fifty male adult Wistar rats were maintained under normal or high-fat diet during 20 weeks. The HFD group received oral clonidine, rilmenidine, LNP 599 or vehicle. Functional microcirculation was evaluated by intravital videomicroscopy and the structural was studied using histochemical analysis. We concluded that the modulation of sympathetic activity reverses the capillary rarefaction in the skeletal muscle and left ventricle in an experimental model of MS in rats

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Edwards, Jeffrey Earl. "THE TRANSPORT AND MODULATION OF HIV PROTEASE INHIBITORS INTO THE RAT CENTRAL NERVOUS SYSTEM AND MILK." UKnowledge, 2004. http://uknowledge.uky.edu/gradschool_diss/468.

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The objective of this dissertation is to study the mechanism by which HIV protease inhibitors enter into the central nervous system (CNS) and breast milk of rats, and what effects MDR modulators have on the distribution and metabolism of HIV protease inhibitors. The transporter P-glycoprotein (P-gp) has been shown to limit the distribution of HIV protease inhibitors into the CNS of rodents. This thesis examined the effects of GF120918, an MDR modulator, on the CNS distribution of amprenavir, an HIV protease inhibitor, in rats. GF120918 significantly increased the unbound CNS concentrations of amprenavir without altering the unbound blood concentrations of amprenavir. The results of these studies show that GF120918 can inhibit P-gp at the blood brain barrier (BBB) to increase the unbound CNS concentration of amprenavir and potentially other HIV protease inhibitors. Many first generation MDR modulators inhibited both P-gp transport and CYP3A metabolism. Therefore, a principal goal of this thesis was to determine if GF120918 could selectively inhibit P-gp transport without inhibiting CYP3A metabolism. Using in vitro (human) and in vivo (rat) studies, GF120918 selectively inhibited P-gp at the BBB without inhibiting CYP3A metabolism. The transporter MRP1 has been shown to both transport HIV protease inhibitors and expressed in the CNS. Studies contained in the thesis have shown that mrp1 is not localized to the BBB of rats, therefore, mrp1 is unlikely to play a significant role in the distribution of HIV protease inhibitors into the CNS of rats. The distribution of nelfinavir, an HIV protease inhibitor, into rat breast milk was studied in the thesis as a first approach in understanding the extent to which HIV protease inhibitors can accumulate into milk. The concentration of nelfinavir in rat milk was approximately half that of plasma. P-gp protein expression was detected in lactating rat mammary tissue. However, GF120918 showed no effect on the distribution of nelfinavir into rat milk suggesting that P-gp does not play a significant role in the distribution of HIV protease inhibitors into milk.

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Niemelä, R. (Raija). "Imaging of salivary glands and assessment of autonomic nervous system function in primary Sjögren's syndrome." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514272757.

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Abstract The purpose of the present study was to find reliable non-invasive methods for imaging salivary glands and diagnosing primary Sj?gren's syndrome (SS) and to evaluate autonomic function and central nervous system (CNS) disorders in patients with primary SS. The patient population consisted of consecutive patients with primary SS, who fulfilled the International classification criteria for primary SS, from the Division of Rheumatology, Department of Internal Medicine in Oulu University Hospital. Magnetic resonance (MR) imaging and MR sialography of parotid glands were performed on 27 patients and 7 healthy controls and ultrasonography (US) of major salivary glands on 27 patients, 27 healthy controls, and 27 symptomatic controls with sicca symptoms or salivary gland swellings without SS. MR imaging and US showed heterogeneous parenchyma or adipose degeneration of the gland in 81% and 78% of patients, respectively. MR sialography showed ductal system changes, narrowings and dilatations, or cavities in 96% of patients. One healthy control and 2 symptomatic controls had abnormal findings of parotid or submandibular glands on US. Other controls had normal findings. The diagnostic specificity of US was 94%. Parenchymal structural changes on MR imaging and US were associated with anti-Ro/SSA positivity and weakly with the focus score index, but not with salivary or tear secretion, age, disease duration, or features of systemic activity of the disease, such as hypergammaglobulinemia or systemic complications. A comprehensive package of cardiovascular tests, including 24-hour heart rate variability, baroreflex sensitivity test with phenylephrine, Valsalva manoeuvre, deep breathing tests, and active orthostatic test, were conducted on 30 patients and 30 healthy, age and sex-matched, randomly selected population-based controls. No signs of autonomic dysfunction were found in patients compared to controls in any of the tests. The test results were not associated with saliva or tear secretion, age, disease duration, or clinical features of systemic activity of the disease. A case of severe inflammatory CNS disease associated with primary SS was described, and an investigation of the relevant literature was made. Though inflammatory CNS disease is a possible complication of primary SS, there is no consensus regarding its prevalence or significance in the literature. Diagnostics and treatment are empiric. In conclusion, MR imaging, MR sialography, and US yield such a definitive picture of the glandular changes in primary SS that they are promising alternatives for invasive examinations in the diagnostics of primary SS. Comprehensive cardiovascular tests revealed no signs of autonomic dysfunction in patients with primary SS compared to general population.

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Day, Brian Keith. "MICROELECTRODE ARRAY STUDIES OF NORMAL AND DISEASE-ALTERED L-GLUTAMATE REGULATION IN THE MAMMALIAN CENTRAL NERVOUS SYSTEM." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/235.

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L-glutamate (Glu) is the major excitatory neurotransmitter in the mammalian central nervous system. Monitoring extracellular Glu is critical to understanding Glu regulation to discriminate physiological and pathological roles. To overcome the limitations of previous in vivo extracellular Glu studies, we developed Glu selective microelectrode arrays with better spatial and temporal resolutions than commonly used techniques like microdialysis. We used these microelectrode arrays to characterize basal and potassium-evoked Glu neurotransmission in the normal rat brain. We then investigated disease-related Glu alterations in a rat model of Parkinson's disease and normal Glu regulation in young and aged rhesus monkeys. In the normal anesthetized rat striatum and frontal cortex, basal Glu was regulated by active release and uptake mechanisms, fully TTX-dependent, and measured at ~2 micromolar levels. Potassium-evoked Glu kinetics were fast, concentration-dependent, and rapidly reproducible at 15-20 seconds intervals. In the unilateral 6-hydroxydopamine-lesioned rat, there were significant bilateral increases in potassium-evoked Glu release in the striatum and frontal cortex compared to hemisphere-matched non-lesioned rats. Ipsilateral striatal effects may have been related to DA loss, while contralateral striatal effects and the bilateral frontal corticaleffects may have resulted from parkinsonian neurotransmitter changes or bilateral neuranatomical connectivity, especially in the cortex. There were also alterations in Glu kinetics in the nucleus accumbens in both non-lesioned and lesioned rats. With appropriate technological and methodological modifications, we successfully recorded normal Glu signaling in anesthetized nonhuman primates in the operating room. Fast potassium-evoked Glu signals were recorded in the motor cortex of all monkeys, and Glu ejections showed robust Glu uptake in the motor and frontal cortices of all monkeys. These findings are comparable to initial rat studies. Slow evoked Glu kinetics and high basal Glu levels with oscillatory behavior were recorded in the frontal cortex. The primary age-related differences between monkeys were the nearly ten-fold increases in the volumes of Glu ejected needed in the aged monkey to achieve amplitude-matched signals in the motor and frontal cortices and a decreased uptake rate in the motor cortex. Preliminary work with excised human tissue and future plans for patient-oriented research and clinical applications are discussed.

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Jansson, Björn. "Models for the Transfer of Drugs from the Nasal Cavity to the Central Nervous System." Doctoral thesis, Uppsala University, Department of Pharmacy, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3905.

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The blood-brain barrier restricts the access of many compounds, including therapeutic agents, to the brain. Several human studies indicate that nasal administration of hydrophilic compounds, such as peptides, can bypass the blood-brain barrier. The aims of this thesis were to develop and refine models for this direct nose-to-brain transfer.

In a mouse model, [³H]-dopamine was given as a unilateral nasal dose. The resulting radioactivity in the ipsilateral olfactory bulb was significantly higher than that in the contralateral bulb and peaked at 4 h. Tape section autoradiography showed that the radioactivity was concentrated in the olfactory nerve layer and the glomerular layer of the olfactory bulb. The olfactory transfer of dopamine was also studied in vitro. At a lower donor concentration, the mucosal-to-serosal dopamine permeability was higher than the serosal-to-mucosal permeability, but at a higher concentration, the permeability coefficients were similar. Together, these results suggest that the olfactory transfer of dopamine has an active component.

Olfactory transfer of fluorescein-labeled dextran through the epithelium and deeper tissues was studied in a rat model, which enabled visualization of the transfer using fluorescence microscopy. Although the epithelial transfer appeared to be mainly intracellular, transfer in the following deeper tissues was extracellular. Without altering the route of uptake, a gellan gum formulation enhanced the uptake of fluorescein dextran. The enhancing effect was considered likely to be the result of an increased residence time in the nasal cavity.

In conclusion, dopamine and fluorescein-labeled dextran were identified as suitable model compounds for the study of olfactory drug transfer mechanisms and the influence of drug formulation. Two new in vitro models of olfactory transfer were compared. Also, a rat model, which enabled the visualization of the entire nose-to-brain transfer, was developed.

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Field, Evelyn F., and University of Lethbridge Faculty of Arts and Science. "Sex differences in movement organization II : the organization of sex differences in movement during food protection, contact righting, skilled reaching and vertical exploration in the rat : the role of gonadal steroids, body morphology, and the central nervous system." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2006, 2006. http://hdl.handle.net/10133/14.

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Whether there are sex differences in the kinematic organization of non-reproductive behaviors is rarely addressed. In this thesis, evidence is presented that male and female rats organize their posture and stepping differently during a food protection task, contact righting, skilled reaching, and vertical rearing. Neonatal gonadal steroid exposure can alter sex-typical patterns of movement organization. Whether these differences are due to sex differences in body morphology or central nervous system (CNS) was also addressed using gravid females and tfm males. The results reveal that sex differences in movement are CNS based. Furthermore, the expression and choice of sex-typical patterns of movement can be altered by CNS injury. Finally, evidence is presented that sex differences in movement organization are also present in marsupials and insects. The implications of these results for our understanding of the evolution of sex differences in CNS anatomy and behavior will be discussed.
xvi, 249 leaves : ill. ; 28 cm.

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Cassolla, Priscila. "Importância do tecido adiposo marrom na ativação da termogênese induzida pela injeção central do C75, um inibidor da ácido graxo sintase." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17134/tde-24092012-155205/.

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C75, um inibidor sintético da ácido graxo sintase, causa anorexia e perda de peso em roedores, mas os mecanismos envolvidos com esses efeitos ainda não são totalmente conhecidos. A hipótese testada nesse trabalho foi que o tecido adiposo marrom (TAM), um órgão com importante função no controle da termogênese, poderia estar envolvido nos efeitos mediados pelos inibidores da ácido graxo sintase. Para isso, ratos Wistar foram submetidos ao implante de cânula no ventrículo lateral direito seguido, ou não, pela desnervação simpática cirúrgica do TAM. Sete dias após, C75 (150 g/7,5 L), cerulenina, um inibidor natural da ácido graxo sintase, (150 g/7,5 L) ou RPMI (veículo) foi administrado nos animais com privação alimentar de 24 horas. Foi demonstrado que uma única injeção intracerebroventricular de C75 reduziu a ingestão alimentar no primeiro dia e induziu perda de peso por dois dias. Além disso, as análises de telemetria mostraram que o C75 promoveu um rápido aumento na temperatura corporal interna, maior taxa de estoque de calor de 30 minutos a 6 horas da administração, e um aumento na dissipação de calor por 4 horas. A desnervação do TAM atenuou os efeitos do C75 sobre a regulação térmica bem como seu efeito sobre o peso corporal e a ingestão alimentar. Em paralelo, o C75 induziu aumento na temperatura do TAM (até 8 horas após a injeção), no conteúdo de noradrenalina e na atividade da citocromo c oxidase mitocondrial e da expressão do RNAm da UCP-1 no tecido. Todos esses efeitos foram abolidos com a desnervação simpática do TAM. Tal como o C75, a cerulenina, também induziu um aumento na temperatura corporal interna e do TAM, o qual também foi abolido pela desnervação do TAM. A atividade locomotora espontânea não foi alterada por nenhum inibidor da ácido graxo sintase. A imunohistoquímica para c-Fos revelou que o C75 aumentou o número de células imunorreativas a c-Fos na área pré-óptica, núcleo paraventricular, dorsomedial do hipotálamo, ventromedial do hipotálamo, locus coeruleus e rafe pálida, regiões que estão envolvidas com a regulação central da temperatura. Estes dados sugerem um papel do TAM no aumento da temperatura corporal evocado pelos inibidores da ácido graxo sintase e provêm novos mecanismos para explicar a hipofagia e o aumento do gasto energético observados com a administração desses compostos.
C75, a synthetic inhibitor of fatty acid synthase, causes anorexia and weight loss in rodents, but the underlying mechanisms are not totally known. Thus, the hypothesis tested in this work was that brown adipose tissue (BAT), an organ with important role for control of thermogenesis, could be involved in the anti-obesity effects of fatty acid synthase inhibitors. To address this issue, Wistar rats were submitted to cannula implant into right lateral ventricle and following, or not, by surgical sympathetic denervation of BAT. Seven days later, C75 (150g/7.5L), cerulenin, a natural fatty acid synthase inhibitor, (150 g/7.5 L) or RPMI (vehicle) was administered in 24h-fasted animals. It was demonstrated that a single intracerebroventricular injection of C75 decreased the food intake on the first day, and induced weight loss for two days. Furthermore, telemetry analyzes shown that the C75 induced a rapid increase in core body temperature, a higher heat storage rate from 30 minutes until 6 hours of injection, and an increase in heat dissipation for 4 hours. The BAT denervation attenuated the thermoregulatory effects of C75 as well as its effect on body weight and food intake. In parallel, C75 induced an increase in BAT temperature (up to 8 hours of the injection), higher content of norepinephrine, and an increase in the activity of cytochrome c oxidase and mRNA expression of UCP-1 in the tissue. All these effects were abolished by sympathetic denervation. Like C75, the central administration of cerulenin also induced an increase in the BAT and core body temperature, which was also abolished by BAT denervation. The spontaneous locomotor activity was not altered by any fatty acid synthase inhibitor. The immunohistochemistry for c-Fos revealed that the C75 increased numbers of Fos-immunoreactive cells in preoptica area, paraventricular nucleus, dorsomedial hypothalamus, ventromedial hypothalamus, locus coeruleus and raphe pallidus, regions which are involved in the central thermoregulation. These data implicate a role for BAT in the fatty acid synthase inhibitors-evoked increase in body temperature and provide new mechanisms to explain hypophagia and increased energy expenditure observed with the administration of these compounds.

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Oliveira, Larissa Resende. "Disfunção autonômica cardíaca e expressão de FOS em núcleos do bulbo após indução de dor crônica difusa não-inflamatória em ratos." Pós-Graduação em Ciências Fisiológicas, 2013. http://ri.ufs.br:8080/xmlui/handle/123456789/3970.

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Fibromyalgia (FM) is characterized by chronic non-inflammatory widespread pain (CWP) and changes in sympathetic function. In attempt to elucidate the pathophysiological mechanisms of FM we used a well-established CWP animal model. We aimed to evaluate changes in cardiac autonomic balance and baroreflex function in response to CWP induction in rats. Therefore, it was used 30 male Wistar rats (250-350 g) with 2 to 3 months. CWP was induced by two injections of acidic saline (pH 4.0, n=16) five days apart into the left gastrocnemius muscle, whereas control animals were injected twice with normal saline (pH 7.2, n = 14). To evaluate changes in cardiovascular responses, one day after the second injection of acidic saline (n=8) or normal saline (n=6) animals were instrumentated to blood pressure recordings and posterior analysis of pulse interval (PI) and systolic arterial pressure (SAP) variability, and spontaneous baroreflex sensitivity (BRS) was performed. To determine the involvement of areas of the CNS (NTS , RVLM and CVLM ), two days after the second injection of acidic saline (n=8) or normal saline (n=8) animals were anesthetized, perfused, the brains removed and cut in a cryostat. The brain sections were subjected to immunofluorescence protocol for Fos protein. Results are expressed as mean ± SEM. Differences between groups were analyzed using by t test, paired and unpaired. Values of p < 0.05 were considered statistically significant. After induction of CWP, there was an increase of power in the low frequency (LF) band of PI spectrum (12.75±1.04 nu), a decrease in the high frequency (HF) band (87.25±1.04 nu) and an increase of LF/HF ratio (0.16±0.01), when compared to control animals (7.83±1.13 nu LF; 92.16±1.13 nu HF; 0.08±0.01 LF/HF). In addition, there was an increase of power in the LF band of SAP spectrum (7.93±1.39 mmHg2) when compared to control animals (2.97±0.61 mmHg2). BRS was lower in acidic saline injected rats (0.59±0.06 ms/mmHg) when compared to control animals (0.71±0.03 ms/mmHg). By immunofluorescence , we found that in all investigated areas the percentage of Fos immunoreactive cells was significantly higher ( p < 0.001) in saline acidic compared to neutral saline group. Our results showed that induction of CWP in rats shifts cardiac sympathovagal balance towards sympathetic predominance and decreases BRS, data which corroborate findings in humans with FM, and also that activation of NTS, CVLM and RVLM appears to indicate the involvement of these areas in an attempt to control the cardiac autonomic dysfunction.
A fibromialgia (FM) é caracterizada por dor muscular crônica difusa não-inflamatória (DMCD) e mudanças na função simpática. No intuito de elucidar os mecanismos fisiopatológicos da FM, foi utilizado um modelo animal de dor crônica difusa bem estabelecido na literatura. Desta forma, o objetivo do estudo foi avaliar a modulação autonômica cardíaca e a função do barorreflexo, em resposta à indução de dor muscular crônica difusa em ratos. Para tanto, foram utilizados 30 ratos Wistar machos (250 a 350g) com 2 a 3 meses. A DMCD foi induzida por duas injeções de solução salina ácida (pH 4,0, n=16) com cinco dias de intervalo, no músculo gastrocnêmio esquerdo, enquanto que os animais controle foram injetados duas vezes com solução salina neutra (pH 7,2, n=14). Para avaliar as alterações nas respostas cardiovasculares, um dia após a segunda injeção de solução salina ácida (n=8) ou salina neutra (n=6) os animais foram instrumentados para gravações da pressão arterial, e posterior análise da variabilidade do intervalo de pulso (IP) e da pressão arterial sistólica (PAS), como também da sensibilidade espontânea do barorreflexo (SBR) foi realizada. Para avaliar a ativação de neurônios em núcleos do Bulbo envolvidos com a modulação autonômica cardíaca (NTS, RVL e CVL), dois dias após a segunda injeção de salina ácida (n = 8) ou de solução salina normal (n=8), os animais foram anestesiados, perfundidos, o cérebro removido e cortado num criostato. As secções do cérebro foram submetidas ao protocolo de imunofluorescência para a proteína Fos. Os resultados são expressos como média ± EPM. Diferenças entre os grupos foram analisados pelo teste t, pareado e não-pareado. Valores de p < 0,05 foram considerados estatisticamente significativos. Após a indução de dor crônica difusa nos ratos (n=8), as variações do intervalo de pulso apresentaram maior oscilação em baixa frequência (LF) (12,75±1,04 un), menor oscilação em alta frequência (HF) (87,25±1,04 un) e maior valor da relação LF/HF (0,16±0,01), quando comparadas ao grupo controle (n=6) (7,83±1,13 un LF; 92,16±1,13 nu HF; 0,08±0,01 LF/HF). Em adição, houve maior oscilação em LF da pressão arterial sistólica (PAS) (7,93±1,39 mmHg), comparado ao grupo controle (2,97±0,61 mmHg). A sensibilidade espontânea do barorreflexo foi menor nos ratos injetados com salina ácida (0,59±0,06 ms/mmHg) quando comparada ao grupo controle (0,71±0,03 ms/mmHg). Através da imunofluorescência, observou-se que em todas as regiões investigadas a porcentagem de células imunorreativas à Fos foi significativamente maior (p<0,001) no grupo salina ácida, em comparação ao grupo salina neutra. Nossos resultados mostraram que a indução da DCMD em ratos desloca o balanço simpatovagal cardíaco em direção a uma predominância simpática e diminui SBR, dados que corroboram achados em seres humanos com FM, e ainda, que a ativação de neurônios do NTS, CVL e RVL parece indicar o envolvimento dessas áreas na modulação da disfunção autonômica cardíaca.

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Xu, Kui. "The Central Nervous System Aspects of Cardiac Arrest and Resuscitation in a Rat Model of Global Ischemia." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270689501.

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46

Newell, Miranda E. "The connection between emotion, brain lateralization, and heart-rate variability /." Download the thesis in PDF, 2005. http://www.lrc.usuhs.mil/dissertations/pdf/Newell2005.pdf.

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Coutinho, Pedro Ricardo de Mesquita. "Avaliação do efeito do tacrolimo e da eritropoetina na lesão medular experimental em ratos." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5140/tde-08122015-095337/.

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Os efeitos farmacológicos da eritropoetina (EPO) e do tacrolimo (FK 506) têm sido investigados no tratamento da lesão medular, mas são escassos os trabalhos que avaliam a interação entre essas drogas. Neste estudo experimental, 60 ratos Wistar foram submetidos a lesão contusa da medula espinal produzida pelo sistema NYU Impactor. Os animais foram divididos em cinco grupos, sendo: Controle, que recebeu soro fisiológico; EPO, que recebeu eritropoetina; o EPO + FK 506 recebeu EPO associada ao tacrolimo; o FK 506 recebeu tacrolimo. Todas as drogas e o soro fisiológico foram administrados por via intraperitoneal. O grupo Sham foi submetido à lesão medular, mas não recebeu nenhuma droga. Os animais foram avaliados quanto à recuperação da função locomotora em sete diferentes momentos pelo teste de BBB no 2o, 7o, 14o, 21o, 28o, 35o e 42o dias após lesão contusa na medula espinal. No 42o dia, foi realizada avaliação eletrofisiológica dos animais que, logo após, foram sacrificados para análise dos achados histológicos da medula lesionada. Nosso projeto experimental não revelou diferenças na recuperação da função locomotora, nas análises histológica e eletrofisiológica nos animais submetidos ao tratamento farmacológico com eritropoetina e com tacrolimo, após contusão medular torácica
The pharmacological effects of erythropoietin (EPO) and tacrolimus (FK 506) have been investigated in the treatment of spinal cord injuries, but there are few studies that evaluate the interaction between these drugs. In this experimental study, 60 Wistar rats were submitted to contusion spinal cord injury produced by the NYU Impactor system. The animals were divided into five groups: Control, which received saline only; EPO, which received erythropoietin; EPO + FK 506, which received EPO associated with tacrolimus; and the group FK 506, which received tacrolimus. All drugs and saline were administered intraperitoneally. The Sham group underwent spinal cord injury, but did not receive any drug. The animals were evaluated for recovery of locomotor function in seven different times by the BBB test, in the 2nd, 7th, 14th, 21st, 28th, 35th and 42nd days after spinal cord injury. In 42 days, electrophysiological evaluation was performed, and the animals were, shortly after, sacrificed for histological analysis of the injured spinal cord. Our experimental study did not reveal significant differences in the recovery of locomotor function, nor in the histological and electrophysiological analysis in animals treated with erythropoietin and tacrolimus after thoracic spinal cord injury

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Levine, Richard. "Evaluation of the Brainstem Spinal Cord Preparation in the Neonatal Rat as a Model for Prenatal Nicotine Exposure." The University of Arizona, 2012. http://hdl.handle.net/10150/623649.

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Class of 2012 Abstract
Specific Aims: The goal of this project was to evaluate the use of a preparation of the brainstem and spinal cord of neonatal rats that has been widely used for observing and quantifying central nervous activity, as well as the response to pharmacological manipulation. To achieve this, we specifically aimed to remove the intact brainstem and spinal cord of newborn rats, and develop a preparation that would maintain physiological function and allow for recording of electrical activity. Methods: Multiple dissections were performed on neonatal rats. Conditions during the dissections were controlled to maintain physiological function. Once removed, the intact brainstem and spinal cord was placed in a preparation that allowed for manipulation and access to nerve rootlets. Finally, glass suction electrodes were used to record electrical activity directly from the nerve rootlets. Once recorded, the data were stored on a hard drive for further analysis. Main Results: We were successful in isolating the intact brainstem and spinal cord in neonatal rats while maintaining physiological conditions and nervous activity. The preparation allowed for easy access to nerve roots as well as customization for different experiments. We were also successful in recording nerve activity in the preparation and collection of data for use in future experiments Conclusions: We conclude that the brainstem spinal cord preparation described in this study is a valuable tool that allows for recording and analysis of nerve activity, and specifically for measurement of respiratory motor output. This is a preparation that can be used in a variety of experiments that attempt to observe or quantify the activity of central nerve cells and allows for pharmacological interventions that could be applied in various experiments.

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Hu, Ying. "Optic nerve regeneration in adult rat." University of Western Australia. School of Anatomy and Human Biology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0080.

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[Truncated abstract] There is limited intrinsic potential for repair in the adult human central nervous system (CNS). Dysfunction resulting from CNS injury is persistent and requires prolonged medical treatment and rehabilitation. The retina and optic nerve are CNSderived, and adult retinal ganglion cells (RGCs) and their axons are often used as a model in which to study the mechanisms associated with injury, neuroprotection and regeneration. In this study I investigated the effects of a variety of strategies on promoting RGC survival and axonal regeneration after optic nerve injury, including the use of reconstructed chimeric peripheral nerve (PN) grafts, gene therapy, and intraocular application of pharmacological agents and other factors . . . C3 transferase is an enzyme derived from Clostridium botulinum that inactivates Rho GTPase. Because SC myelin contains MAG and PN also contains CSPGs, I tested the effects of intraocular injection of a modified form of C3 (C3-11), provided by Dr Lisa McKerracher (CONFIDENTIAL data, under IP agreement with Bioaxone Therapeutic, Montreal) on RGC axonal regeneration into PN autografts. My results showed that there was significantly more RGC survival and axonal regeneration in PN autografts after repeated intraocular injection of C3. I also tested whether intraocular injections of CPT-cAMP and/or CNTF can act in concert with the C3 to further increase RGC survival and/or regeneration. Results showed that the effect of C3 and CPT-cAMP plus CNTF were synergistic and partially additive. The use of combination therapies therefore offers the best hope for robust and substantial regeneration. The overall results from my PhD project will help determine how best to reconstruct nerve pathways and use pharmacological interventions in the clinical treatment of CNS injury, hopefully leading to improved functional outcomes after neurotrauma.

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Brown, Russell W., Marla K. Perna, Daniel M. Noel, Jamie D. Whittemore, Julia Lehmann, and Meredith L. Smith. "Amphetamine Locomotor Sensitization and Conditioned Place Preference in Adolescent Male and Female Rats Neonatally Treated with Quinpirole." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/6341.

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Neonatal quinpirole treatment has been shown to produce an increase in dopamine D2-like receptor sensitivity that persists throughout the subject's lifetime. The objective was to analyze the effects of neonatal quinpirole treatment on effects of amphetamine in adolescent rats using locomotor sensitization and conditioned place preference procedures. Sprague-Dawley rats were treated with quinpirole (1 mg/kg) or saline from postnatal days (P)1 to P11 and raised to adolescence. For locomotor sensitization, subjects were given amphetamine (1 mg/kg) or saline every second day from P35 to P47 and were placed into a locomotor arena. In female rats, neonatal quinpirole treatment enhanced amphetamine locomotor sensitization compared with quinpirole-free controls sensitized to amphetamine. Male rats demonstrated sensitization to amphetamine, although this was muted compared with female rats, and were unaffected by neonatal quinpirole. For conditioned place preference, subjects were conditioned for 8 consecutive days (P32-39) with amphetamine (1 mg/kg) or saline and a drug-free preference test was conducted at P40. Rats treated with neonatal quinpirole enhanced time spent in the amphetamine-paired context compared with quinpirole-free controls conditioned with amphetamine, but only female controls conditioned with amphetamine spent more time in the drug-paired context compared with saline-treated controls. Increased D₂-like receptor sensitivity appears to have enhanced the behavioral effects of amphetamine, but these effects were more prevalent in adolescent female rats compared with male rats.

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