Dissertations / Theses on the topic 'Mice – Nervous system'
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Tsao, Jack W. "Wallerian degeneration in normal mice and in mutant C57BL/Wld mice." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260174.
Full textLiu, Hern Choon Eugene. "The central nervous system effects of nocistatin : behavioral effects in mice." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611850.
Full textAndersson, Sandra. "Nuclear receptor functions in the central nervous system clues for knockout mice /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-661-1/.
Full textSimpson, Matthew Thomas W. "Caspace-3 deficiency rescues peripheral nervous system defect in pRb nullizygous mice." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6297.
Full textLamprianou, Smaragda. "Biological role of nervous system tyrosine phosphatases revealed by analysis of KO mice." Paris 6, 2007. http://www.theses.fr/2007PA066107.
Full textMarsicano, Giovanni. "Physiological role of the cannabinoid receptor 1 (CB1) in the murine central nervous system." n.p, 2000. http://ethos.bl.uk/.
Full text邱大安 and Tai-on Yau. "Regulation of the mouse hoxb-3 gene in the neural expression domains during embryogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242601.
Full textLee, King-yiu. "The Ret gene in the enteric nervous system expression analysis and generation of ret deficient mice /." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31449669.
Full textStromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.
Full textLee, King-yiu, and 李景耀. "The Ret gene in the enteric nervous system: expression analysis and generation of ret deficient mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31449669.
Full textHo, Wing-lau, and 何穎流. "Investigating neurodegeneration in the retina of tau P301L mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B4833392X.
Full textpublished_or_final_version
Anatomy
Master
Master of Medical Sciences
羅慧詩 and Wai-sze Law. "Conditional knockout of neural cell adhesion molecule L1 in mouse brain." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B42575266.
Full textLaw, Wai-sze. "Conditional knockout of neural cell adhesion molecule L1 in mouse brain." Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/hkuto/record/B42575266.
Full textTanaka, Hisataka. "Conduction properties of identified neural pathways in the central nervous system of mice in vivo." Kyoto University, 2004. http://hdl.handle.net/2433/145280.
Full text0048
新制・課程博士
博士(医学)
甲第11099号
医博第2779号
新制||医||877(附属図書館)
22649
UT51-2004-L896
京都大学大学院医学研究科脳統御医科学系専攻
(主査)教授 大森 治紀, 教授 金子 武嗣, 教授 橋本 信夫
学位規則第4条第1項該当
Colbert, Crystal. "Functional Neural Toxicity and Endocrine Responses in Mice Following Naphthalene Exposure." Thesis, University of North Texas, 2010. https://digital.library.unt.edu/ark:/67531/metadc31529/.
Full textHillard, Kynlee, Matthew Zahner, David Kyle Mounger, Brooke Tipton, and Grayson Jo White. "The effect of leptin on metabolic- and cardiovascular-related pre-sympathetic hypothalamic neurons in mice." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/11.
Full textHullmann, Maja [Verfasser]. "Evaluation of the effects of inhaled nanoparticles on the central nervous system of mice / Maja Hullmann." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1030365237/34.
Full textRoss, Shelley 1973. "Generation and characterization of mice lacking the α4 nicotinic receptor subunit." Monash University, Dept. of Medicine, 2001. http://arrow.monash.edu.au/hdl/1959.1/9180.
Full textChan, Yuk-yee. "Tissue-specific expression of cre recombinase in the developing enteric nervous system of a Hoxb3/cre transgenic mouse strain." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2510116x.
Full textChen, Yuk-shan. "Tissue specific expression studies on a vagal neural crest enhancer element of the mouse Hoxb3 gene in the development of the enteric nervous system /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23424564.
Full textYung, Kin-lam Ken. "Quantification of neuropeptides in the central nervous system of the wobbler mouse during the progression of the motor neuron disease : a study by radioimmunoassay and immunocytochemistry /." [Hong Kong : University of Hong Kong], 1992. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1320502X.
Full text陳玉儀 and Yuk-yee Chan. "Tissue-specific expression of cre recombinase in the developing enteric nervous system of a Hoxb3/cre transgenic mouse strain." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970400.
Full textGautam, Dinesh Chandra. "Analysis of insulin receptor function in the central nervous system by conditional inactivation of its gene in mice." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96492353X.
Full textLi, Yuanfang [Verfasser], and Sabine [Akademischer Betreuer] Steffens. "Arterial wall immunity in hyperlipidemic mice is regulated by the sympathetic nervous system / Yuanfang Li ; Betreuer: Sabine Steffens." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1227840055/34.
Full textBolton, Hall Amanda Nicholle. "HISTOLOGICAL AND BEHAVIORAL CONSEQUENCES OF REPEATED MILD TRAUMATIC BRAIN INJURY IN MICE." UKnowledge, 2016. http://uknowledge.uky.edu/physiology_etds/26.
Full text陳玉珊 and Yuk-shan Chen. "Tissue specific expression studies on a vagal neural crest enhancer element of the mouse Hoxb3 gene in the development of the entericnervous system." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31224088.
Full textBovenkamp, Diane Elizabeth. "Eph receptor tyrosine kinases, nervous system development and angiogenesis, cloning and characterization of Eph receptors from zebrafish and mice." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/NQ54056.pdf.
Full textChaube, Sanjay. "Ubiquitin Expression in the Lumbar Spinal Cord Motoneurons of Postnatal Mice-- an Immunohistochemical Study." Thesis, University of North Texas, 1994. https://digital.library.unt.edu/ark:/67531/metadc332620/.
Full textLowe-Chatham, Janice E. (Janice Elaine). "Effects of 5-hydroxytryptamine on Mouse Lumbar Motor Activity During Postnatal Development." Thesis, University of North Texas, 1998. https://digital.library.unt.edu/ark:/67531/metadc277784/.
Full textBrabb, Thea. "The fate of MBP-specific T cells in MBP TCR transgenic mice /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10853.
Full textMolina, Leandro. "Efeitos do treinamento e destreinamento físico sobre a manuntenção da memória e funcionamento do sistema colinérgico central de camundongos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-16062014-095759/.
Full textThe processes of memory formation involves learning, consolidation and retrieval of information and processes involving neuronal circuits in the cortex, hippocampus and amygdala. The formation of long term memory occurs through the formation of LTP - \"long term potentiation\" that is modulated by multiple neurotransmitter systems, including the cholinergic system. It is known that physical activity increases the production of neurotrophins leading to an improvement of pathological conditions, increases the density of nicotinic receptors on hippocampal cells alfa7. It has been reported that for two weeks detraining leads to the reversion of beneficial cardiovascular effects. This project evaluates the effects of physical training and detraining on swimming on the maintenance of long-term memory of female mice by determining the density of nicotinic receptors alfa7 and neurotrophin BDNF in hippocampus, than showed no significant differences among the groups at work.
Cambon, Karine. "Influence of ApoE polymorphism on synaptic morphometry during aging in the dentate gyrus of ApoE knockout and human ApoE transgenic mice." Thesis, [n.p.], 2000. http://oro.open.ac.uk/19118/.
Full textShewale, Swapnil Vijay. "LOW DOSE NERVE AGENT SARIN CAUSES DILATED CARDIOMYOPATHY AND AUTONOMIC IMBALANCE IN MICE." Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1316090377.
Full text翁建霖 and Kin-lam Ken Yung. "Quantification of neuropeptides in the central nervous system of the wobbler mouse during the progression of the motor neuron disease: a study by radioimmunoassay andimmunocytochemistry." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1992. http://hub.hku.hk/bib/B31210673.
Full textCoiculescu, Olivia Elena. "Mouse cortical cholinergic neurons: Ontogeny of phenotypes in vivo and in vitro." Thesis, University of North Texas, 2005. https://digital.library.unt.edu/ark:/67531/metadc4890/.
Full textFridman, Leticia. "Histopathological Characterization of the Dystrophic Phenotype and Development of Therapeutic Candidates for a Gene Therapy Pre-Clinical Study in Dysferlin Deficient Mice." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/881.
Full textFridman, Leticia. "Histopathological Characterization of the Dystrophic Phenotype and Development of Therapeutic Candidates for a Gene Therapy Pre-Clinical Study in Dysferlin Deficient Mice." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/881.
Full textParviz, Maryam. "Evaluation of Zinc Toxicity Using Neuronal Networks on Microelectrode Arrays: Response Quantification and Entry Pathway Analysis." Thesis, University of North Texas, 2007. https://digital.library.unt.edu/ark:/67531/metadc3928/.
Full textCage, Mary Pauline. "Molecular characterization of mesocorticolimbic brain regions in DBA/2J mice sensitized to the locomotor activating effects of ethanol /." Abstract, 24-page preview and downloadable full-text (PDF format) available to VCU users at:, 2005. http://wwwlib.umi.com/cr/vcu/fullcit?p3196511.
Full textMillward, Jason Michael 1976. "Interferon-gamma and the regulation of neuroinflammation." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115699.
Full textPontes, Renata Bessa. "Envolvimento da endotelina-1, de receptores (TRPV1 E NMDA) e da substÃncia p na neuropatia sensitiva perifÃrica induzida pelo agente antineoplÃsico oxaliplatina." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15621.
Full textIntroduÃÃo: A neurotoxicidade cumulativa à uma toxicidade que pode advir da terapia à base de oxaliplatina (OXL), que à a 3 geraÃÃo de agentes platinos com amplo espectro de atividade antitumoral, incluindo cÃncer colorretal, ovariano e pulmonar. A neurotoxicidade associada à OXL gera uma toxicidade dose-limitante, crÃnica, a neuropatia sensitiva perifÃrica (NSP). Objetivo: Investigar o envolvimento da endotelina-1, de receptores TRPV1 e NMDA e da substÃncia P envolvidos na patogÃnese da neuropatia sensitiva perifÃrica induzida pelo agente antineoplÃsico oxaliplatina. Materiais e mÃtodos: O estudo foi aprovado pelo Comità de Ãtica em Pesquisa Animal da UFC (protocolo n 75/12). Camundongos Swiss machos (20g) foram prÃ-tratados com antagonistas de receptores de endotelina-1 (Bosentana 100mg/kg, VO; BQ-123 e BQ-788 30Âl, intraplantar) e antagonistas do receptor TRPV1 (capsazepina, 5mg/kg, IP), antagonista do receptor NK-1 da Substancia P (apreptanto, 1mg/kg, IP) e antagonista de receptores NMDA (MK-801, 0,5mg/kg, IP) 30 minutos antes da administraÃÃo de OXL (1mg/kg, IV) por 4 semanas e meia. Paralelamente foram realizados testes nociceptivos para avaliar o desenvolvimento da neuropatia sensitiva perifÃrica. A hipernocicepÃÃo foi avaliada pelo teste de imersÃo da cauda (TIC) em Ãgua fria (10ÂC) ou aquecida (43ÂC) e pelo teste Von Frey (HPM). Em seguida, foi realizado imunofluorescÃncia do segmento medular e gÃnglio da raiz dorsal e RT-PCR. Resultados: Como resultados observou-se que com o prÃ-tratamento ao uso de OXL que houve atenuaÃÃo da hiperalgesia da NSP induzida por OXL. Ao realizar a administraÃÃo de antagonistas seletivos de endotelina-1 intraplantar na pata direita observou-se reduÃÃo significativa na hiperalgesia na pata direita (tratada) em comparaÃÃo à pata esquerda (controle). Ao analisar a expressÃo gÃnica para cFos, NK-1 e o receptor de endotelina B, observou-se que houve reduÃÃo significativa da expressÃo dos marcadores no grupo prÃ-tratado com Bosentana ao comparar com o grupo OXL, que demonstrou a expressÃo aumentada para esses marcadores. ConclusÃo: Conclui-se no presente estudo que hà evidÃncias do papel da endotelina-1, de receptores (TRPV1 e NMDA) e da substÃncia P na patogÃnese da NSP induzida pelo agente antineoplÃsico OXL.
Introduction: The cumulative neurotoxicity is a toxicity that can result from oxaliplatin-based therapy (OXL), which is the 3rd generation platinum agent with broad spectrum of antitumor activity, including colorectal, ovarian and lung cancer. Neurotoxicity associated with OXL generates a dose-limiting toxicity, chronic, peripheral sensory neuropathy (NSP). Objective: To investigate the involvement of endothelin-1, TRPV1 receptors and NMDA and substance P involved in the pathogenesis of peripheral sensory neuropathy induced by oxaliplatin antineoplastic agent. Methods: Male Swiss mice (20g) were pre-treated with antagonists of endothelin-1 receptors (Bosentan 100mg / kg orally; BQ-123 and BQ-788 30μl, intraplantar) and TRPV1 receptor antagonists (capsazepine, 5mg / kg , IP), antagonist of NK-1 receptor for substance P (apreptanto, 1 mg / kg, IP), and a NMDA receptor antagonist (MK-801, 0.5mg / kg, IP) 30 minutes before administration of OXL (1mg / kg, IV) for 4.5 weeks. Parallel nociceptive tests performed to assess the development of peripheral sensory neuropathy. The hyperalgesia assessed by the tail immersion test (ICT) in cold water (10Â C) or warm (43Â C) and test Von Frey (HPM). Then it was performed spinal segment, and the dorsal root ganglion immunofluorescence and RT-PCR the Ethics Committee approved the study for Animal Research UFC (Protocol 75/12). Results: The results observed when using the antagonists, as a pretreatment to the use of OXL there was attenuation of the induced hyperalgesia (NSP) OXL. Upon administration of selective antagonists of endothelin in the right paw was significant reduction in paw hyperalgesia in the right (treated) compared to the left paw (control). By analyzing the gene expression of cFos, NK-1 and endothelin B receptor, it was observed that there was significant reduction of expression of the markers in pre-treated bosentan group versus OXL group that showed increased expression for these markers. Conclusion: It was concluded in this study that there is evidence of the role of endothelin-1 receptors (TRPV1 and NMDA) and substance SP in the pathogenesis of NSP induced antineoplastic agent OXL.
Bacurau, Aline Villa Nova. "Caracterização fenotípica do músculo esquelético na cardiomiopatia induzida por hiperatividade simpática." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-12112007-165712/.
Full textHeart failure (HF) is a clinical syndrome with high incidence and bad prognostic, characterized by fatigue, dyspnea, and increased intolerance to exercise. These changes are not only related to the cardiovascular tissue, but are at least in part, consequence of morphofunctional alterations in skeletal muscles. To the present study it was used mice lacking both ?2A/?2C AR subtypes (KO) which develop cardiomyopathy induced by sympathetic hyperactivity, associated to clinical signals of HF and 50% of mortality at seven months of age. The aim of the present study was characterize the phenotype of skeletal muscle by functional and morphological evaluations in KO before (three months of age) and during the HF progression (five and seven months of age). Skeletal muscle alterations due HF were observed only at seven months of age. The alterations were characterized by vascular rarefaction, muscular atrophy, increase in glycolitic fibers percentage and reduction of maximal activity of citrate synthase and contributed with early fatigue observed in this model, and consequently, exercise intolerance. The results of present study suggest that KO mice present morphofunctional changes in skeletal muscles in a similarly to others models of HF and in patients that have this syndrome. Therefore, consisting in an excellent experimental model to future studies related to therapeutic strategies to minimize the skeletal muscle changes due HF
Oli-Rijal, Sabnam. "Determination of Dissociation Constants for GABAA Receptor Antagonists using Spontaneously Active Neuronal Networks in vitro." Thesis, University of North Texas, 2005. https://digital.library.unt.edu/ark:/67531/metadc4911/.
Full textSimões, Gustavo Ferreira 1978. "Plasticidade sináptica em motoneurônios alfa medulares de camundongos MDX tratados com fator estimulador de colônias granulocitárias (GCSF)." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316412.
Full textTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Atualmente, muito se sabe sobre o acometimento muscular na DMD, mas poucos estudos estão voltados para os efeitos no Sistema Nervoso Central (SNC), mais especificamente no microambiente do motoneurônio medular. Sabe-se que durante a evolução da doença, o terminal axonal, na junção neuromuscular, entra em um ciclo de denervação (retração) e reinervação (brotamento). A possibilidade de modulação do MHC I se apresenta como uma nova estratégia de influenciar positivamente o processo de plasticidade sináptica após lesões do Sistema Nervoso Periférico (SNP) e SNC. Tal modulação pode ser realizada através da utilização ou desenvolvimento de drogas específicas. O fator estimulador de colônias glanulocitárias (G-CSF) é uma glicoproteína que foi descrita há mais de vinte anos, possui aprovação do ANVISA (Agência Nacional de Vigilância Sanitária) e é comumente utilizada para tratar neutropenia, ou para transplantes de medula óssea. O GCSF possui um efeito neuroprotetor aparentemente multimodal, incluindo-se a atividade anti-apoptóptica em neurônios, regeneração da vascularização, efeito antiinflamatório e estimulação de neurogênese endógena, sendo capaz de atuar efetivamente no processo de regeneração do sistema nervoso. No presente trabalho, foram utilizados camundongos MDX. Os camundongos foram distribuídos em 4 grupos (axotomia + G-CSF; Axotomia; Controle + G-CSF e Controle), com n=10. Incluiu-se para imunoistoquímica o grupo placebo, onde os animais receberam uma dose diária de 200?m, via subcutânea, de glicose a 25%. Nossos resultados indicam que redução de sinapses nos motoneurônios alfamedulares e aumento da astrogliose circunjacente aos neurônios alfa-medulares, seja decorrente da desconexão parcial entre o orgão alvo e o corpo neuronal durante o período de ciclos de degeneração/regeneração muscular que ocorrem a partir das primeiras semanas de vida nos camundongos MDX. Estes ciclos podem repercutir retrogradamente nos corpos celulares dos motoneurônios alfa-medulares, provocando uma série de alterações denominadas cromatólise. A axotomia do nervo isquiático resulta num aumento significativo da expressão de MHC I nas duas linhagens estudadas. Contudo, nos animais MDX, este aumento é menor, comparativamente à linhagem C57BL/10. Quando tratados com G-CSF a expressão de MCH I ficou maior em relação aos grupos não tratados e, isso pode indicar um papel ativo da droga no potencial regenerativo após a lesão. Também podemos sugerir que, apesar dos animais MDX apresentarem uma menor função motora em relação aos animais controle, os resultados indicam que o tratamento com G-CSF é capaz de reduzir os efeitos inflamatórios e atuar positivamente no processo de regeneração nervosa periférica após esmagamento do nervo isquiático
Abstract: Currently, much is known about the muscular involvement in DMD, but few studies have focused on the effects on the central nervous system (CNS), specifically in the microenvironment of spinal motor neurons. It is known that during the course of the disease, the axon terminal at the neuromuscular junction, enters a cycle of denervation (retraction) and reinnervation (sprouting). The possibility of modulation of MHC I presents itself as a new strategy to positively influence the process of synaptic plasticity after injury Peripheral Nervous System (PNS) and CNS. Such modulation may be accomplished through the use or development of special drugs. The granulocyte colony-stimulating factor (G-CSF) is a glycoprotein which was first described more than twenty years, has approval from ANVISA (Agência Nacional de Vigilância Sanitária) and is commonly used to treat neutropenia, or bone marrow transplants. The G-CSF has a multimodal neuroprotective effect l, including the anti-apoptotic activity in neurons, regeneration of vascularization, anti-inflammatory effect and stimulation of endogenous neurogenesis, being able to act effectively in the process of regeneration of the nervous system. In this study, we used MDX mice. The mice were divided into 4 groups (axotomy + G-CSF; axotomy, Control + G-CSF and Control), with n = 10. Included immunohistochemistry to the placebo group, where the animals received a daily dose of 200?m, subcutaneously, glucose 25%. Our results indicate that reduction of synapses in the alpha motoneurosn and increased astrogliosis , either due to partial disconnection between the target organ and the neuronal body during the cycles of degeneration /regeneration muscle that occur from first weeks of life in MDX mice. These cycles can pass retrogradely in alpha motoneurons cell bodies, causing a series of changes called chromatolysis. The sciatic nerve axotomy results in a significant increase of MHC I expression in both strains studied. However, in MDX strain, this increase is smaller, compared to C57BL/10. After treatment with G-CSF the expression of MCH I got bigger compared to untreated groups, and this may indicate an active role in the regenerative potential of the drug after injury. Also we suggest that while the animals present MDX a smaller motor function compared to control animals, the results indicate that treatment with G-CSF is capable of reducing the inflammatory effects and act positively on peripheral nerve regeneration process after nerve crush sciatic. Also our results indicate that treatment with G-CSF is able to reduce the inflammatory effects and act positively on peripheral nerve regeneration process after nerve crush sciatic
Doutorado
Anatomia
Doutor em Biologia Celular e Estrutural
Moraes, Oscar Albuquerque de. "Avaliação da modulação autonômica cardiovascular de camundongos diabéticos não obesos." Universidade Nove de Julho, 2013. http://bibliotecadigital.uninove.br/handle/tede/1146.
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Introduction: It is known that diabetes is associated with autonomic dysfunction and this is a severe complication that increases the risk of cardiovascular mortality. The non-obese diabetic mice (NOD) is an experimental model of type 1 diabetes which develops insulitis at the 4th week and diabetes between the 14th and the 20th week of life. However, data about autonomic function in these mice remain scarce. Objective: To investigate the cardiovascular autonomic profile of NOD mice. Methods: Female mice (24-28 week old) were divided in two groups: NOD (n=6) and control (n=6, swiss mice). NOD mice with glycemia ≥300 mg/dl were used in this study. Heart rate variability (HRV) was evaluated in time and frequency domains and also through symbolic analysis. Were also analyzed the variability of the blood pressure, and baroreflex sensitivity by means of the bradycardic and tachycardic responses induced by infusion of phenylephrine and sodium nitroprusside. Student t test for independent samples and Pearson's correlation coefficient were used for statistical analyses. The data were described as means and standard error. Results: The heart rate and arterial pressure were similar between the groups, however HRV (total variance of RR interval: NOD = 21.07 ± 3.75 vs. C = 42.02 ± 6.54 ms2) and RMSSD (NOD = 4.01 ± 0.32 vs. C = 8.28 ± 0.97 ms), a vagal modulation index, were lower in NOD group when compared to control group. Moreover, the low frequency component was higher in NOD group (normalized LF: NOD = 61.0 ± 4.0 vs. C = 20.0 ± 4.0%), while the high frequency of HR component was lower in NOD compared with the control group (normalized HF: NOD = 39.0 ± 4.0% vs. C = 80.0 ± 4.0%). Similarly, the 0V pattern of symbolic analysis, indicative of sympathetic activity, was increased in NOD group when compared to the control group (NOD = 11.9 ± 1.4 vs. C = 6.06 ± 0.90%) and the 2LV pattern, indicative of parasympathetic activity, was reduced in the NOD group (NOD = 7.98 ± 1.3 vs. C = 21.2 ± 3.36%). Both responses to arterial pressure changes, tachycardic (NOD = 3.01 ± 0.72 vs. C = 4.54 ± 0.36 bpm/mmHg) and bradycardic (NOD = 2.49 ± 0.31 vs. C = 3.43 ± 0.33 bpm/mmHg) were lower in NOD when compared to the control group. A negative correlation between the indices of vagal modulation (RMSSD, normalized high frequency component and 2LV pattern of symbolic analysis) and blood glucose levels was also observed. Conclusions: The NOD mice present cardiovascular autonomic dysfunction and that is probably associated with glycemic levels.
Introdução: O diabetes está associado com disfunção autonômica e esta é uma grave complicação que eleva o risco de mortalidade cardiovascular. O camundongo não obeso diabético (NOD) é um modelo experimental de diabetes tipo 1 que desenvolve insulinite na quarta semana de vida e diabetes entre a 14ª e 20ª semana de vida. Contudo, dados sobre a função autonômica cardiovascular em camundongos NOD permanecem escassos. Objetivos: Investigar a função autonômica cardiovascular do camundongo NOD. Métodos: Camundongos fêmeas (24-28 semanas de vida) foram divididas em dois grupos: NOD (n = 6) e controle (C, camundongo suiço, n=6). Foram incluídos no grupo NOD animais com glicemia igual ou superior a 300 mg/dl. Foi avaliada a variabilidade da frequência cardíaca no domínio do tempo e da frequência e também por meio de análise simbólica. Além disso, foram avaliados a variabilidade da pressão arterial, bem como a sensibilidade barorreflexa, por meio das respostas bradicárdicas e taquicárdicas induzidas pela infusão de fenilefrina e nitroprussiato de sódio. Para análise estatística foi utilizado o teste t de Student para amostras independentes e o coeficiente de correlação de Pearson. Os dados foram descritos como média e erro padrão. Resultados: A frequência cardíaca e a pressão arterial foram similares entre os grupos, no entanto a variabilidade da frequência cardíaca (variância do intervalo de pulso: NOD = 21,07 ± 3,75 vs. C = 42,02 ± 6,54 ms2) e o RMSSD (NOD = 4,01 ± 0,32 vs. C = 8,28 ± 0,97 ms), um índice de modulação vagal, foram menores no grupo NOD quando comparados ao grupo controle. Além disso, o componente de baixa frequência foi maior no grupo NOD (BF normalizado: NOD = 61,0 ± 4,0 vs. C = 20,0 ± 4,0%), enquanto que o componente de alta frequência foi menor no grupo NOD quando comparado com o grupo controle (AF normalizado: NOD = 39,0 ± 4,0% vs. C = 80,0 ± 4,0%). De forma semelhante, na análise simbólica o padrão 0V, indicativo da atividade simpática, estava aumentado no grupo NOD em comparação com o grupo controle (NOD= 11,9 ± 1,4 vs. C = 6,06 ± 0,90%) e o padrão 2LV, indicativo da atividade parassimpática, estava reduzido no grupo NOD (NOD = 7,98 ± 1,3 vs. C = 21,2 ± 3,36%). Ambas as respostas reflexas comandadas pelos barorreceptores, taquicárdica (NOD = 3,01 ± 0,72 vs. C = 4,54 ± 0,36 bpm/mmHg) e bradicárdica (NOD = 2,49 ± 0,31 vs. C = 3,43 ± 0,33 bpm/mmHg) foram menores no grupo NOD quando comparadas com o grupo controle. Ainda, observamos uma correlação negativa entre os índices de modulação vagal (RMSSD, componente de alta frequência normalizado e padrão 2LV da análise simbólica) e os níveis glicêmicos. Conclusão: Os camundongos NOD apresentam disfunção autonômica cardiovascular e essa disautonomia está associada com os níveis glicêmicos.
Pan-Montojo, Francisco, Oleg Anichtchik, Yanina Dening, Lilla Knels, Stefan Pursche, Roland Jung, Sandra Jackson, et al. "Progression of Parkinson's Disease Pathology is Reproduced by Intragastric Administration of Rotenone in Mice." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-185435.
Full textMaduna, Tando Lerato. "Vasoactive intestinal peptide (VIP) controls the development of the nervous system and its functions through VPAC1 receptor signalling : lessons from microcephaly and hyperalgesia in VIP-deficient mice." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ009/document.
Full textThe studies carried out during my PhD demonstrate that VIP-deficient mice suffer from microcephaly and as well as white matter deficits mainly due to the absence of maternal VIP during embryogenesis, Placental secretion of VIP is dependent on T lymphocytes and could be altered in pathologies of the immune system. Moreover, our data links VIP deficiency to sensory alterations, specifically, the nociceptive system. Thus, it is possible that early developmental defects and hypersensitivity to mechanical and cold stimuli are two manifestations of the same pathology. This hypothesis was reinforced following analysis of spontaneous firing patterns of neurons in the sensory thalamus of anesthetized adult males. Neurons from VIP-KO mice are hyperactive, which suggests aberrant local processing of nociceptive input or that the inhibitory inputs from local interneuron networks is reduced
Sicot, Géraldine. "Conséquences pathologiques des expansions CTG sur le système nerveux central d’un modèle murin de la dystrophie myotonique de Steinert : approches moléculaires, protéomiques et cellulaires." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T084/document.
Full textMyotonic dystrophy type 1 (DM1) is the most frequent inherited muscular disorder in adults. Although traditionally regarded as a muscle disease, DM1 presents debilitating neurological manifestations. DM1 is an autosomic dominant disease caused by the abnormal expansion of a CTG triplet within the 3’UTR of the DMPK gene. Many molecular aspects of the DM1 are mediated by a trans effect of the expanded DMPK transcripts, whose accumulation leads to splicing deregulation in many tissues. Despite recent progress in the understanding of DM1 pathogenesis in muscle and central nervous system (CNS), the detailed molecular disease mechanism operating in the brain is still poorly understood. In order to investigate the pathophysiology, our laboratory has generated DMSXL transgenic mice expressing DMPK transcripts containing large CUG expansions in many tissues. DMSXL mice mimic important features of the DM1, notably in the CNS, showing behaviour as well as electrophysiological abnormalities. Therefore, this mouse line represents an excellent tool to investigate the toxic effects of the mutation in the CNS. Taking advantages of this transgenic model, I have first explored the trans effect of the toxic RNA and the extent of DM1-associated spliceopathy in the CNS. Interestingly, some splicing defects were region-specific, and their severity did not increase with the age of the DMSXL mice. My data demonstrate that CUG-containing RNAs have a wide deleterious effect and deregulate alternative splicing in many areas of the CNS. In addition to splicing abnormalities in cerebellum, DMSXL mice also displayed deficits in cerebellum-dependant motor coordination. Plus, DMSXL cerebellum showed electrophysiological abnormalities, suggesting cerebellar dysfunction and more precisely Purkinje cell dysfunction. In the search for the cellular populations showing the greatest susceptibility to RNA toxicity in the cerebellum, I have found extensive foci accumulation as well as pronounced splicing defects in the Bergman glia, surrounding Purkinje cells, in DMSXL and DM1 patients cerebellum. In order to identify molecular pathways and mechanisms behind the behaviour and electrophysiological abnormalities detected, I have performed a global proteomics approach and found a severe decrease in the expression of a glial glutamate transporter GLT1/EAAT2, suggesting that DM1 causes cerebellum dysfunction, through abnormal glutamate metabolism. Global proteomic analysis of DMSXL cerebellum also identified expression and post-translational changes of several proteins involved in calcium signalling. Missplicing of different transcripts involved in calcium metabolism reinforces the idea of calcium dysfunction in the neuropathogenesis of the DM1. To study the effects of toxic RNA on calcium homeostasis and flux, I have established and characterised a brain cell model of DM1. DMSXL primary astrocyte cultures allowed me to show the mislocalisation of the glutamate receptor GRIN1/NMDAR1, as well as abnormal calcium responses to stimulation. Despite recent therapeutic advances in muscle, we do not know the CNS efficiency of the therapeutic strategies currently being developed. To address this problem, I have used the DM1 astrocyte cell model to validate in cellulo a therapeutic strategy aiming to restore the activity of the endogenous splicing factor MBNL1. My thesis work provided a significant step in the understanding of the DM1 pathology in the CNS. My results revealed for the first time signs of cerebellum dysfunction in DM1, as well as signs of calcium homeostasis deregulation in the SNC. My work contributed to better understand the pathological mechanisms of DM1, the brain pathways and cell types most susceptible to toxic RNA. In the long term, my data will contribute to the rational development of therapeutic strategies targeting precise and deleterious molecular events
Wolf, Amy. "In Vitro Studies of Nuclear Changes in Mammalian CNS Neurons Subjected to Rapid Acceleration Impact Injury." Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc278044/.
Full textPan-Montojo, Francisco, Oleg Anichtchik, Yanina Dening, Lilla Knels, Stefan Pursche, Roland Jung, Sandra Jackson, et al. "Progression of Parkinson's Disease Pathology is Reproduced by Intragastric Administration of Rotenone in Mice." PloS ONE, 2010. https://tud.qucosa.de/id/qucosa%3A29010.
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