Dissertations / Theses on the topic 'Rats – Nervous system'
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Chai, Hong. "Survival and regeneration of spinal motoneuron after ventral root avulsion in adult rat /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?
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袁秋菊 and Qiuju Yuan. "Effects of neurotrophic factors on motoneuron survival following axonal injury in developing rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B42128705.
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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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Yuan, Qiuju. "Effects of neurotrophic factors on motoneuron survival following axonal injury in developing rats." Click to view the E-thesis via HKUTO, 2001. http://sunzi.lib.hku.hk/hkuto/record/B42128705.
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Hooper, Justin Shane. "Cardiovascular Effects Evoked by Airway Nociceptive Reflexes in Healthy and Cardiovascular Diseased Rats." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6258.
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Acute inhalation of airborne pollutants alters cardiovascular function and has been shown to have its greatest affects on individuals with pre-existing cardiovascular disease. Evidence suggests that pollutant-induced activation of airway sensory nerves via the gating of ion channels is critical to these systemic responses. Here, we have investigated the cardiovascular responses evoked by inhalation of AITC (TRPA1 agonist) and capsaicin (TRPV1 agonist) in healthy Sprague Dawley (SD) and Wistar Kyoto (WKY) rats, and cardiovascular diseased Spontaneously Hypertensive (SH) rats. Inhalation of the agonists by healthy SD and WKY rats caused significant bradycardia, atrio-ventricular (AV) block and prolonged PR-Intervals. Inhalation of TRP agonists caused differential cardiovascular responses in the cardiovascular diseased SH rats, such that the TRP agonists evoked brady-tachy with AV block and premature ventricular contractions (PVCs). Bradycardic responses to AITC were inhibited by the TRP channel blocker ruthenium red and the muscarinic antagonist atropine, but atropine did not prevent the tachycardic responses seen in the SH rats. Adrenergic inhibition with atenolol prevented the tachycardic responses, but did not prevent the bradycardic responses evoked by AITC in the SH rats. In healthy rats, AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase, while evoking hypertension in the SH rats. Atropine accentuated the hypertensive phase in all animals, while preventing the hypotension in the healthy animals. In all animals, AITC-evoked heart rate responses were not abolished by terazosin, the [U+F061]1 adrenoceptor inhibitor, which prevented the hypertensive responses. Anesthetics had profound effects on AITC-evoked bradycardia and AV block, which was abolished by urethane, ketamine and isoflurane. Nevertheless, AITC inhalation caused bradycardia and AV block in paralyzed and ventilated rats following pre-collicular decerebration. In conclusion, we provide evidence that activation of TRP channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in healthy rats via reflex modulation of the autonomic nervous system (ANS), and that these effects are exacerbated in cardiovascular diseased rats.
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Lau, Chi-yan Jane. "Brain derived neurotrophic factors (BDNF) and seprafilm?adhesion barrier on sciatic nerve regeneration in rats." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42924789.
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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 CasattiResumo: 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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Häidkind, Riina. "Monoaminergic mechanisms in mood-associated behaviours and neurochemistry in rats /." Tartu : Tartu University Press, 2004. http://dspace.utlib.ee/dspace/bitstream/10062/704/5/Haidkind.pdf.
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柴宏 and Hong Chai. "Survival and regeneration of spinal motoneuron after ventral root avulsion in adult rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B3124158X.
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Lau, Chi-yan Jane, and 劉至欣. "Brain derived neurotrophic factors (BDNF) and seprafilm® adhesion barrier on sciatic nerve regeneration in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42924789.
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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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Dolatshad, Nazanin Fatima. "Expression analysis of GDNF family of neurotrophic factors and their receptors in the postnatal, adult and ageing gut and bladder of rats." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288967.
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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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Grant, Michael Peter. "Nerve-target interactions in the developing sympathetic nervous system of the rat. Regulation of rat sweat gland secretory function by acetylcholine." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1059494178.
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Sauls, Bryan Auston. "Integrated modulation of sympathetic tone in the microcirculation by oxygen, adenosine, and nitric oxide." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2025.
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Thesis (Ph. D.)--West Virginia University, 2001.Title from document title page. Document formatted into pages; contains xii, 195 p. : ill. Vita. Includes abstract. Includes bibliographical references.
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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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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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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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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 - MScBackground: 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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Kwok, Hon Hung. "Immunolesioning in the rat brain." HKBU Institutional Repository, 1999. http://repository.hkbu.edu.hk/etd_ra/234.
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Li, Shengxiu. "The role of glial cells in the survival and axonal regeneration of retinal ganglion cells /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20897650.
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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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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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Rollins, Korynne Sierra. "Bradykinin does not acutely sensitize the reflex pressor response during hindlimb skeletal muscle stretch in decerebrate rats." Thesis, Kansas State University, 2018. http://hdl.handle.net/2097/38617.
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Master of ScienceDepartment of Kinesiology
Steven Copp
Hindlimb skeletal muscle stretch (i.e., selective activation of the muscle mechanoreflex) in decerebrate rats evokes reflex increases in blood pressure and sympathetic nerve activity. Bradykinin has been found to sensitize mechano-gated channels through a bradykinin B2 receptor-dependent mechanism. Moreover, bradykinin B2 receptor expression on sensory neurons is increased following chronic femoral artery ligation in the rat (a model of simulated peripheral artery disease). We tested the hypothesis that, in decerebrate, unanesthetized rats, the injection of bradykinin into the arterial supply of a hindlimb would acutely augment (i.e., sensitize) the increase in blood pressure and renal sympathetic nerve activity (RSNA) during hindlimb muscle stretch to a greater extent in rats with a ligated femoral artery than in rats with freely perfused femoral arteries. The pressor response during static hindlimb muscle stretch was compared before and after the hindlimb arterial injection of 0.5 µg of bradykinin. The injection of bradykinin itself increased blood pressure to a greater extent in “ligated” rats (n=10) than in “freely perfused” rats (n=10). The increase in blood pressure during hindlimb muscle stretch, however, was not different before compared to after bradykinin injection in either freely perfused (control: 14±2, post-bradykinin: 15±2 mmHg, p=0.62) or ligated (control: 15±3, post-bradykinin: 14±2 mmHg, p=0.80) rats. Likewise, the increase in RSNA during stretch was not different before compared to after bradykinin injection in either group of rats. We conclude that bradykinin did not acutely sensitize the pressor response during hindlimb skeletal muscle stretch in either freely perfused or ligated decerebrate rats.
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Jin, Ying. "Neuronal survival and axonal regeneration of the lateral vestibular nucleus in rats after spinal cord injury /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19918847.
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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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Sizemore, Rachel J., and n/a. "Innervation of cholinergic interneurons in the striatum of the rat." University of Otago. Department of Anatomy & Structural Biology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090915.155925.
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Cholinergic interneurons are relatively rare neurons in the rat striatum. These sparsely distributed neurons display a synchronous pause in their tonic firing pattern during reward-related learning. It has been hypothesised that a specialised fast-conducting crossed-corticostriatal pathway is involved in synchronising the pause in tonic firing of these interneurons. This study aimed to detail the innervation of cholinergic interneurons by mapping their proximal and distal inputs and to describe the innervation of the crossed-corticostriatal pathway in male Wistar rats. In vivo electrophysiological recording methods were used to label single crossed-corticostriatal neurons but inadequately labeled their axons. Thus, an anterograde neuronal tracing study was conducted. Biotinylated dextran amine (BDA; 1.2 [mu]l) was pressure-injected into the left cerebral hemisphere. Six days later, the rat was perfused-fixed and the brain sectioned. BDA-labelled axons were traced to both the ipsilateral and contralateral striata. Cholinergic interneurons in the right striatum were double-immunolabelled using an optimised protocol including a polyclonal rabbit anti-m2-muscarinic receptor antibody and a monoclonal goat anti-choline acetyltransferase antibody. All sections were processed for transmission electron microscopy. Serial ultrathin sections were montaged and distal (from non BDA-labelled tissue) and proximal synapses were each mapped separately. A reconstructed distal dendrite from a cholinergic interneuron, located 225 [mu]m from the soma, was analysed. It had an average width of 1 .25[mu]m and 0.726 synapses per [mu]m. This was compared to dendrites in the same tissue and from BDA-labelled tissue. Two dendrites were presumed to be distal profiles of either cholinergic or somatostatin interneurons, while the third was thought to belong to another interneuronal cell type. In terms of surface area, there were less somal synapses compared to those made onto the distal dendrite of the cholinergic interneuron. Somal synapse counts were similar to those reported previously from our laboratory, where symmetric synapses were most common. Crossed-corticostriatal BDA-labelled axons were found to course across proximal dendrites and somas of immunolabelled cholinergic interneurons. Varicosities from these axons were found in close proximity to proximal dendrites and somas of cholinergic interneurons. Of all cholinergic interneurons in an adjacent section, 77% showed closely associated proximal varicosities. Of these, 76% of varicosities were associated with the soma, 11% to proximal dendrites and 13% to both locations. Twenty-nine BDA-labeled axons were analysed using transmission electron microscopy. Most were observed making asymmetric synaptic contact with unlabelled spines. In two cases spines were traced to medium spiny projection neurons. Two axon segments were seen touching the proximal regions of separate cholinergic interneurons. At these contact sites interrupted membrane thickenings were observed. It is proposed here that synapses may form at these sites during reward-related learning. However labelling of the contact sites with a postsynaptic marker would be necessary to confirm their synaptic nature. The current study has gathered information about the distal and proximal innervation patterns of these neurons and described the termination pattern of the crossed-corticostriatal pathway in relation to these neurons for the first time. These findings support the crossed-corticostriatal pathway as one possible anatomical substrate for synchronising the pause response on both sides of the brain.
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Löf, Elin. "Conditional and non-conditional reward-related responses to alcohol : nicotinic mechanisms /." Göteborg : Institute of Neuroscience and Physiology, Section for Pharmacology, the Sahlgrenska Academy at Göteborg University, 2006. http://hdl.handle.net/2077/742.
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Zhang, Yi. "Studies of heparanase (HPA) gene expression, cellular localization and functions in neural tissues of the rat." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634061.
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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
Graduate
31
Eskow, Karen Louise. "The essential role of the rostral raphe nuclei in movement control in the L-DOPA-treated, hemiparkinsonian rat." Diss., Online access via UMI:, 2008.
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32
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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Neo, Phoebe Suat-Hong, and n/a. "Theta activations associated with goal-conflict processing : evidence for the revised "behavioral inhibition system"." University of Otago. Department of Psychology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090309.160549.
Full textAbstract:
In the theory of the Behavioral Inhibition System (BIS), Gray and McNaughton (2000) classified events that produce or inhibit goal-directed behaviour into two affective categories: approach versus avoidance. We experience goal-conflict when approximately equal but incompatible approach and avoidance tendencies are concurrently activated. Gray and McNaughton (2000) proposed goal-conflict as a class of mechanisms separable from "simple" mechanisms: Goal-conflict effects are maximal when incompatible approach and avoidance tendencies are balanced, simple effects are maximal when either approach or avoidance tendencies predominate.
Gray and McNaughton (2000) saw the hippocampus as a key nexus for resolving goal conflict by recursive amplification of the subjective value of punishment, thereby increasing avoidance tendencies. Rodent hippocampal theta (4-12 Hz) is necessary (but not sufficient) for correct and efficient transmission of hipppocampal outputs. The BIS theory is fundamentally an animal model. It is not clear if a human BIS exists in the same form. Record human hippocampal (4-12 Hz) activity from the scalp is unlikely. However, during goal-conflict resolution, cortically generated theta recorded from the scalp could be modulated by human hippocampal theta. Therefore, superficially recorded 4-12 Hz theta spectra power was used to assess if specific goal-conflict processing activity could be detected in humans.
Human goal-conflict processing was assessed in four experiments: the Stop-Signal Task (SST), an existing experimental task, and three variations of a task termed "Choice", created for this thesis. Across experiments, three key conditions were created. Approach and avoidance were balanced in the intermediate condition (maximal goal-conflict). Net approach and avoidance predominated in the adjacent conditions respectively (minimal goal-conflict). Goal-conflict was assessed as the difference between activity in the intermediate condition and the average activity across the adjacent conditions (via extraction of the orthogonal quadratic trend for significance testing).
Goal-conflict increased activations consistently at F8, above the right frontal cortex. Increase in task dependent goal-conflict activations were also observed at F7, Fz and F4 above the frontal cortex, and T3, T4, T5 and T6 above the temporal cortex. Activations within the human theta frequency range (4-7 Hz) were consistently detected in the Choice tasks. In the SST, activations spanned the conventional human theta (4-7 Hz) and alpha (8-12 Hz) frequencies. In the Choice tasks, higher conflict theta at T3, T5 and F8 predicted increased avoidance.
Taken together, the findings support Gray and McNaugthon�s (2000) views that a) goal-conflict is a class of mechanism separable from simple approach and avoidance; b) goal-conflict processing recruits and increases cortical rhythmic activity within the same frequency range as rodent hippocampal theta (4-12 Hz); and goal-conflict is resolved by increasing the subjective value of punishment, thereby increasing avoidance tendencies. Although speculative, the current work identified a right inferior frontal gyrus neural circuit for slower, and a presupplementary motor area circuit for faster behavioral inhibition during goal-conflict resolution. These circuits are not explicit in the current BIS model.
34
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/.
Full textAbstract:
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.
35
Towell, Todd L. "Electrophysiologic detection of the neurotoxic effects of acrylamide and 2,5-hexanedione in rats." Thesis, This resource online, 1994. http://scholar.lib.vt.edu/theses/available/etd-06232009-063513/.
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Yuan, Qiuju, and 袁秋菊. "The plasticity of hypothalamic magnocellular system following axonal damage by hypophysectomy in developing and adult rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30301117.
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李勝修 and Shengxiu Li. "The role of glial cells in the survival and axonal regeneration of retinal ganglion cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238932.
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38
Barnum, Christopher John. "The role of neuroinflammation in L-dopa-induced dyskinesia." Diss., Online access via UMI:, 2008.
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39
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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Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Full textAbstract:
The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
41
Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Full textAbstract:
Doctor of PhilosophyThe general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
42
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.
Full textAbstract:
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.
43
Zhang, Yi, and 張怡. "Studies of heparanase (HPA) gene expression, cellular localization andfunctions in neural tissues of the rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634061.
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Salazar, Eduardo. "Effects of Whisker-Trimming on GABAA Receptors in S1 Cortex." Thesis, University of North Texas, 2004. https://digital.library.unt.edu/ark:/67531/metadc4576/.
Full textAbstract:
A number of studies have shown that sensory deprivation is associated with selective decreases in GABA, GAD, and GABA receptors, in deprived areas of visual and somatosensory cortex. Those studies focused on layer 4, a recipient of direct thalamocortical sensory input. However, supragranular layers 2/3 have been recently identified as a major locus of functional plasticity in sensory deprivation and long-term potentiation. To examine whether GABAA receptors in layers 2/3 are affected by sensory deprivation, rats had mystacial vibrissae in middle row C or rows ABDE trimmed for 6 weeks beginning in early adulthood. Layers 2/3 above the deprived and adjacent whisker barrels were located in tangential sections, using patterns of radial blood vessels as fiducial marks. In deprived whisker barrel columns, [3H]muscimol binding to GABAA receptors decreased by 12.8% ± 1.2 (P < 0.001) in layers 2/3 and 11.4% ± 1.2 (P<0.001) in layer 4. Altered levels of GABAA α1 subunit (Fritschy et al., 1994) were indicated by reduced optical density of immunostaining, both in deprived layers 2/3 (6.4% ± 0.7; P< 0.001) and in layer 4 (3.4% ± 1.0; P < 0.005). Interestingly, Nissl staining density also decreased in deprived layers 2/3 (12.7% ± 1.8 P < 0.001) and in 4 (6.0 ± 0.7 (P < 0.001). The percent decreases were greater in layers 2/3 than in 4 for both GABAA α1 (P < 0.05) and Nissl substance (P < 0.005). The present results suggest that down-regulation in GABAA receptors may underlie the physiological signs of disinhibition observed in neurons of layer 2/3 and 4 in deprived whisker barrel columns.
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Binoki, Daniella Harumy. "Alterações cardiopulmonares induzidas em ratos saudáveis após a instilação nasal subcrônica de suspensão aquosa de material particulado fino em concentração ambiental." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-03092010-112925/.
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Há diversas evidências epidemiológicas de correlações positivas entre indicadores de morbidade e mortalidade pulmonar e cardiovascular e aumentos na concentração atmosférica de MP2,5 (material particulado fino). O objetivo deste trabalho foi avaliar os efeitos da exposição subcrônica de MP2,5 sobre o tônus cardíaco autonômico, a inflamação pulmonar e sistêmica; o estresse oxidativo e a homeostase sanguínea, após oito semanas de repetidas instilações nasais de suspensão aquosa de MP2,5 da cidade de São Paulo em concentração ambiental. Dividiram-se os animais em dois grupos: salina e MP2,5 e avaliaram-se os seguintes parâmetros: frequência cardíaca (FC), variabilidade da frequência cardíaca (VFC), pressão arterial sistólica (PA), hemograma, contagem de plaquetas e reticulócitos, fibrinogênio plasmático, tempo de protrombina (TP), tempo de tromboplastina parcialmente ativada (TTPA), mielograma, citologia do lavado broncoalveolar (LBA), análise histopatológica e imuno-histoquímica (15-F2tisoprostano e -actina) de pequenas arteríolas pulmonares e coronarianas. Não houve alterações na FC e na PA (p > 0,05). Houve interação estatisticamente significante entre grupos e semanas em relação à VFC. O SDNN (desvio padrão dos intervalos R-R normais), a r-MSSD (raiz quadrada da média dos quadrados das diferenças sucessivas entre intervalos R-R normais adjacentes) e a AF (alta frequência) do grupo MP2,5 aumentaram significativamente na 7ª semana em comparação à 1ª semana (p < 0,05), enquanto a BF (baixa frequência) não se alterou (p > 0,05). A porcentagem de macrófagos no LBA do MP2,5 diminuiu significativamente (p < 0,05). Não se observaram alterações no sangue, mielograma e análise histopatólogica e imuno-histoquímica dos vasos (p > 0,05). Concluiu-se que a exposição subcrônica pela instilação nasal de suspensão aquosa de MP2,5 em concentração ambiental causou inflamação pulmonar tênue e alterou o equilíbrio cardíaco autonômicoThere are several epidemiological evidences of positive correlation between indicators of pulmonary and cardiovascular morbidity and mortality and increases of PM2.5 (fine particulate matter) air concentration. The aim of this experiment was to evaluate the effects of subchronic exposure of PM2.5 on cardiac autonomic tone, pulmonary and systemic inflammation, oxidative strees and blood homeotasis of healthy rats after eight weeks of repeated nasal instillations of suspended PM2.5 from Sao Paulo city in environmental concentration. Rats were divided in two groups: saline and PM2.5. The following parameters were evaluated: heart rate (HR), heart rate variability (HRV), systolic blood pressure (BP), hemogram, platelets and reticulocytes count, plasmatic fibrinogen, prothrombin time (PT), activated partial thromboplastin time (APTT), bone marrow cells, bronchoalveolar lavage cells (BAL), histopathological and immunohistochemical analysis (15-F2tisoprostane and -actin) of pulmonary and coronary small arterioles. No changes were detected in HR and BP (p > 0.05). There were a statistically significant interaction between groups and weeks in relation to HRV. SDNN (standard deviation of normal RR intervals), r-MSSD (square root of the mean of the squared differences between adjacent normal RR intervals) and HF (high frequency) of PM2.5 group significantly increased on 7th week compaired to 1st week (p < 0.05), while LF (low frequency) did not alter (p > 0.05). BAL macrophages porcentage of PM2.5 group significantly decreased (p < 0.05). No alterations were observed in blood, bone marrow cells, histopathological and immunohistochemical analysis of vessels (p > 0.05). We concluded that subchronic exposure by nasal instillation of aquous suspension of PM2.5 in environmental concentration caused tenuous pulmonary inflammation and altered cardiac autonomic balance
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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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Jin, Ying, and 金瑩. "Neuronal survival and axonal regeneration of the lateral vestibular nucleus in rats after spinal cord injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237113.
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Wu, Xiaoyan. "Effects of dietary potassium depletion in salt-dependent hypertension, the kidney, electrolyte balance, and sympathetic nervous system in Dahl rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0019/NQ28087.pdf.
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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 tratadosThis 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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Moore, Jack. "Autoradiographic Localization of Carbachol-Induced Second Messenger Response in the Rat Spinal Cord Following Inflammation." Thesis, University of North Texas, 2002. https://digital.library.unt.edu/ark:/67531/metadc3125/.
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This study examined central mechanisms of persistent pain using an autoradiographic technique to localize phosphoinositide hydrolysis (PI) in the rat spinal cord dorsal horn. The lateral half of laminae I-II showed the highest levels of baseline PI turnover and carbachol-stimulated PI turnover in normal animals as well as after inflammation. Inflammation resulted in increased baseline PI turnover in this region of the ipsilateral (76%) and contralateral (65%) dorsal horns. Carbachol increased PI turnover in this region in normal rats (55%) and following inflammation (ipsilateral: 46%, contralateral: 45%). The absolute magnitudes of these increases were 1.85, 2.71, and 2.51 nCi/mg, respectively. The results of this study demonstrate the involvement of PI turnover in neural mechanisms of persistent pain, and provide evidence for the involvement of cholinergic systems in this process. Because spinal cholinergic systems have been reported to be anti-nociceptive, the present results appear to reflect an upregulation of anti-nociceptive activity in response to inflammation. Thus, the spinal cholinergic system may be a regulatory site within the anti-nociceptive pathway, and may provide an attractive target for the development of new therapeutic agents.