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1
D'Rozario, Robin H. J. "The effect of peripheral nerve injury on the trigeminal ganglion in the rat /." Title page, Contents and Precis only, 1985. http://web4.library.adelaide.edu.au/theses/09DM/09dmd793.pdf.
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Brown, Heidi Catherine. "Macrophages and the nervous system." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320118.
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Hoshi, Rosangela Akemi [UNESP]. "Variabilidade da freqüência cardíaca como ferramenta de análise da função autonômica: revisão de literatura e comparação do comportamento autonômico e metabólico em recuperação pós-exercício." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/87318.
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O sistema nervoso autônomo (SNA) desempenha um papel importante na regulação dos processos fisiológicos do organismo humano tanto em condições normais quanto patológicas. Dentre as técnicas utilizadas para sua avaliação, a variabilidade da frequência cardíaca (VFC) tem emergido como uma medida simples e não-invasiva dos impulsos autonômicos, representando um dos mais promissores marcadores quantitativos do balanço autonômico. A VFC descreve as oscilações no intervalo entre batimentos cardíacos consecutivos (intervalos R-R), assim como oscilações entre frequências cardíacas instantâneas consecutivas. Trata-se de uma medida que pode ser utilizada para avaliar a modulação do SNA sob condições fisiológicas, tais como em situações de vigília e sono, diferentes posições do corpo, treinamento físico, e também em condições patológicas. Mudanças nos padrões da VFC fornecem um indicador sensível e antecipado de comprometimentos na saúde. Uma alta variabilidade na frequência cardíaca é sinal de boa adaptação, caracterizando um indivíduo saudável, com mecanismos autonômicos eficientes, enquanto que, baixa variabilidade é frequentemente um indicador de adaptação anormal e insuficiente do SNA, implicando a presença de mau funcionamento fisiológico no indivíduo. Diante da sua importância como um marcador que reflete a atividade do SNA sobre o nódulo sinusal e como uma ferramenta clínica para avaliar e identificar comprometimentos na saúde, este artigo revisa aspectos conceituais da VFC, dispositivos de mensuração, métodos de filtragem, índices utilizados para análise da VFC, limitações de utilização e aplicações clínicas da VFC.
Autonomic nervous system (ANS) plays an important role in the regulation of the physiological processes of the human organism during normal and pathological conditions. Among the techniques used in its evaluation, the heart rate variability (HRV) has arising as a simple and non-invasive measure of the autonomic impulses, representing one of the most promising quantitative markers of the autonomic balance. The HRV describes the oscillations in the interval between consecutive heart beats (RR interval), as well as the oscillations between consecutive instantaneous heart rates. It is a measure that can be used to assess the ANS modulation under physiological conditions, such as wakefulness and sleep conditions, different body positions, physical training and also pathological conditions. Changes in the HRV patterns provide a sensible and advanced indicator of health involvements. Higher HRV is a signal of good adaptation and characterizes a health person with efficient autonomic mechanisms, while lower HRV is frequently an indicator of abnormal and insufficient adaptation of the autonomic nervous system, provoking poor patient's physiological function. Because of its importance as a marker that reflects the ANS activity on the sinus node and as a clinical instrument to assess and identify health involvements, this study reviews conceptual aspects of the HRV, measurement devices, filtering methods, indexes used in the HRV analyses, limitations in the use and clinical applications of the HRV.
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Pereira, Francisco Carlos. "Estudo experimental e quantitativo da reinervação muscular após regeneração de nervos no interior de próteses tubulares." Universidade de São Paulo, 1993. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-16052012-152634/.
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Objetivamos o estudo quantitativo e temporal do padrão de inervação do músculo extensor longo dos dedos (edl), após transecção do nervo ciático em camundongos e reparo imediato pela técnica de tubulização. Assim, o músculo edl apresentou-se desnervado na segunda semana após a tubulização. Todas as fibras musculares do edl estavam reinervados na sexta semana após o implante da protese tubular. Entre a sexta e a quadragesima semanas pós-implante a proporção de fibras musculares do edl com mono e poli-inervação aumentou de 3:1 para 4:1. Na quadragésima semana após o implante do tubo foi atingida a porcentagem máxima (80%) de inervação troncular das placas motoras do edl mono-inervadas. Mesmo com tempos prolongados de sobrevivencia após implante, não houve estabilização do padrão de origem das fibras nervosas que convergiam para as placas poli-inervadas do edl. A mono-inervação troncular foi readquirida por 65% das fibras musculares do edl dos animais tubulizados, padrão encontrado em 100% das fibras musculares do edl dos animais não operados. Os padrões morfometricos de reinervação do músculo edl foram idênticos, a partir do terceiro mes, entre o grupo de animais com secção e tubulização do nervo ciatico e o grupo com simples esmagamento do nervo, evidenciando padrão similar de reinervação muscular a longo prazo.We aimed to study the quantitative and temporal pattern of muscle innervation extensor digitorum longus (EDL), following transection of the sciatic nerve in mice and immediate repair technique for tubing. Thus, the EDL muscle denervation presented in the second week after the tubing. All of the EDL muscle fibers were reinnervated in the sixth week after the implantation of prosthetic tube. Between the sixth and FORTY weeks post-implantation, the proportion of muscle fibers of the EDL with mono-and poly-innervation increased from 3:1 to 4:1. The forty weeks after the implantation of the tube was reached maximum percentage (80%) of trunk innervation of motor endplates of the EDL mono-innervated. Even with prolonged survival times after implantation, there was no stabilization of the pattern of origin of nerve fibers that converged on the plates of poly-innervated EDL. The mono-innervation trunk was regained by 65% of EDL muscle fibers of animals tubularized, pattern found in 100% of EDL muscle fibers of animals not operated. The morphometric patterns of reinnervation of the EDL muscle were identical, from the third month, the group of animals with tubing and resources section of the sciatic nerve and the group with simple nerve crush, showing similar pattern of muscle reinnervation in the long term.
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Fong, Chung-yan Gardian. "A study of motor neuron disease in the community and in a large multigenerational kindred." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37602263.
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Foster, Michelle Tranace. "Central nervous system regulation of fat cell lipid mobilization the role of the sympathetic nervous system /." restricted, 2005. http://etd.gsu.edu/theses/available/etd-11162005-154631/.
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Thesis (Ph. D.)--Georgia State University, 2005.Timothy Bartness, committee chair; Elliott Albers, Ruth Harris , Sarah Pallas, committee members. Electronic text (181 p. : ill.)) : digital, PDF file. Description based on contents viewed July 17, 2007. Includes bibliographical references (p. 148-181).
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Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.
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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.
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Tep-Cullison, Chhavy R. "Distinct roles of p75 regulation on myelination in the peripheral nervous system and central nervous system." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1299179635.
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Rezaie, Payam. "Microglia in the developing nervous system." Thesis, King's College London (University of London), 2003. https://kclpure.kcl.ac.uk/portal/en/theses/microglia-in-the-developing-nervous-system(bf8d0495-ab2c-4d63-8f4c-3572ee29a5f2).html.
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Orike, Nina. "Chemorepulsion in the developing nervous system." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243382.
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Solomon, Thomas. "Central nervous system infections in Vietnam." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340736.
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Zhang, Hui. "Remyelination in the central nervous system." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8095.
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Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhance remyelination. The aim of this thesis was to first characterize a fast and reliable model to study CNS remyelination in vitro, and second to investigate the role of semaphorin 3a (Sema3A) and semaphorin 3f (Sema3F) signaling in CNS remyelination. Various in vivo models have been developed to investigate the pathology of multiple sclerosis, and can be used to test remyelination therapies. However, in vivo models are expensive, animal- and time- consuming. Until now, there has been no well-characterized and robust in vitro model for remyelination study. In this thesis, an ex vivo slice culture system with mouse brain and spinal cord was developed, and characterized by immunofluorescent microscopy and transmission electron microscopy, for CNS remyelination study. Automated (re)myelinating quantification by image pro plus software was developed and validated to provide a fast and reliable way for testing factors that change remyelination efficiency. Two such factors are Sema3A and 3F, which were initially identified as axon guidance cues during development. Sema3A (repulsive) and 3F (attractive) were proved to play a role in oligodendrocyte precursor cell (OPC) migration during development, and hypothesized to be important in remyelination. In this thesis, I investigated the effects and mechanisms for this by adding recombinant SEMA3A or SEMA3F or by knockdown their obligatory receptors Neuropilin (Nrp) 1 and 2, using lentivirus induced miRNAi. Slice culture and primary OPC culture were used to determine the effect on OPC survival, migration, proliferation, differentiation and myelination.
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Grant, James Roger. "Nitrergic signalling in the nervous system." Thesis, University of Sussex, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249111.
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Sisask, Gregor. "Bone Development and the Nervous System." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-99443.
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Zhang, Xiaochun. "Involvement of neuroinflammation in models of neurodegeneration." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1663059561&sid=3&Fmt=2&clientId=18949&RQT=309&VName=PQD.
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Radke, James Melvin. "Studies involving somatostatin systems in the rodent central nervous system." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26518.
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Somatostatin is a neuropeptide found throughout the brain. Several studies have established its anatomical distribution as being quite heterogenous with relatively high concentrations appearing in the limbic and striatal systems. Presently, very little is known about the functions of somatostatin systems in the brain and how they interact with other transmitter systems. The following report is a summary of experiments undertaken to assess the functional and chemical interactions of somatostatin with other neurotransmitter systems.
Previous studies have established that the dopaminergic inputs to the basal ganglia are important for locomotor activity and reward. These systems have also been implicated in several mental and neural diseases such as schizophrenia, depression, and Parkinson’s disease.
In the first experiment, interactions between dopamine and somatostatin systems were examined using paradigms involving behavioural responses to dopamine agonists. Depletion of somatostatin levels by the drug cysteamine was found to attenuate amphetamine- and apomorphine-mediated motor behaviours but not the reinforcing aspects of amphetamine. The second experiment attempted to further characterize the nature of the dopamine-somatostatin interaction by examining the effects of haloperidol, a dopamine antagonist, on central somatostatin levels. Short term treatment with haloperidol decreased striatal somatostatin levels. Long term treatment (8 months) with haloperidol failed to alter somatostatin levels in the caudate-putamen.
Since somatostatin levels appear to be normal in Parkinsonian brains, the effects of MPTP poisoning in mice on central somatostatin levels was also studied to examine the accuracy of this animal model of Parkinson's disease and examine the effects of dopaminergic lesions on somatostatin levels. The results of this experiment indicate that MPTP causes a dose dependent increase in nigral somatostatin levels without altering striatal or cortical levels. These results are in partial disagreement with results obtained from both post-mortem Parkinsonian brains and primates given MPTP, thereby questioning the accuracy of this mouse model of Parkinson's disease.
The final experiment examined the effects of the anticonvulsant-antidepressant carbamazepine on central somatostatin levels in the rat. Although the chemical mechanisms responsible for the therapeutic effects of carbamazepine are unknown, previous studies have suggested that its efficacy in the treatment of both manic-depression and epilepsy may be associated with the ability of this drug to reduce the abnormal somatostatin levels observed in these diseases. In this experiment, neither acute, chronic, nor withdrawal from chronic treatment with carbamazepine were found to alter the levels of somatostatin in rats. The lack of effects of carbamazepine on basal somatostatin levels may indicate somatostatin cells are susceptible to carbamazepine only under pathological situations.
Together, these results are discussed in the context of recent observations of abnormal somatostatin levels in several diseases of the central nervous system and provide some insight into the interactions and functions of somatostatin systems in the normal and abnormal brain.Medicine, Faculty of
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周韋基 and Wai-kei Dominic Chau. "A morphometric study of axon-glial interactions." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31212141.
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Chan, Ching. "Axon-restrictive chondroitin sulfates at the Schwann cell-astroycte interface." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40687296.
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Chau, Wai-kei Dominic. "A morphometric study of axon-glial interactions /." [Hong Kong] : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14801486.
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Bayley, Timothy George. "Imaging calcium dynamics during motor pattern generation and sensory processing in insect nervous systems." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709485.
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Hoshi, Rosangela Akemi. "Variabilidade da freqüência cardíaca como ferramenta de análise da função autonômica : revisão de literatura e comparação do comportamento autonômico e metabólico em recuperação pós-exercício /." Presidente Prudente : [s.n.], 2009. http://hdl.handle.net/11449/87318.
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Orientador: Carlos Marcelo PastreBanca: Luiz Carlos Marques Vanderlei
Banca: Moacir Fernandes de Godoy
Resumo: O sistema nervoso autônomo (SNA) desempenha um papel importante na regulação dos processos fisiológicos do organismo humano tanto em condições normais quanto patológicas. Dentre as técnicas utilizadas para sua avaliação, a variabilidade da frequência cardíaca (VFC) tem emergido como uma medida simples e não-invasiva dos impulsos autonômicos, representando um dos mais promissores marcadores quantitativos do balanço autonômico. A VFC descreve as oscilações no intervalo entre batimentos cardíacos consecutivos (intervalos R-R), assim como oscilações entre frequências cardíacas instantâneas consecutivas. Trata-se de uma medida que pode ser utilizada para avaliar a modulação do SNA sob condições fisiológicas, tais como em situações de vigília e sono, diferentes posições do corpo, treinamento físico, e também em condições patológicas. Mudanças nos padrões da VFC fornecem um indicador sensível e antecipado de comprometimentos na saúde. Uma alta variabilidade na frequência cardíaca é sinal de boa adaptação, caracterizando um indivíduo saudável, com mecanismos autonômicos eficientes, enquanto que, baixa variabilidade é frequentemente um indicador de adaptação anormal e insuficiente do SNA, implicando a presença de mau funcionamento fisiológico no indivíduo. Diante da sua importância como um marcador que reflete a atividade do SNA sobre o nódulo sinusal e como uma ferramenta clínica para avaliar e identificar comprometimentos na saúde, este artigo revisa aspectos conceituais da VFC, dispositivos de mensuração, métodos de filtragem, índices utilizados para análise da VFC, limitações de utilização e aplicações clínicas da VFC.
Abstract: Autonomic nervous system (ANS) plays an important role in the regulation of the physiological processes of the human organism during normal and pathological conditions. Among the techniques used in its evaluation, the heart rate variability (HRV) has arising as a simple and non-invasive measure of the autonomic impulses, representing one of the most promising quantitative markers of the autonomic balance. The HRV describes the oscillations in the interval between consecutive heart beats (RR interval), as well as the oscillations between consecutive instantaneous heart rates. It is a measure that can be used to assess the ANS modulation under physiological conditions, such as wakefulness and sleep conditions, different body positions, physical training and also pathological conditions. Changes in the HRV patterns provide a sensible and advanced indicator of health involvements. Higher HRV is a signal of good adaptation and characterizes a health person with efficient autonomic mechanisms, while lower HRV is frequently an indicator of abnormal and insufficient adaptation of the autonomic nervous system, provoking poor patient's physiological function. Because of its importance as a marker that reflects the ANS activity on the sinus node and as a clinical instrument to assess and identify health involvements, this study reviews conceptual aspects of the HRV, measurement devices, filtering methods, indexes used in the HRV analyses, limitations in the use and clinical applications of the HRV.
Mestre
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Gatt, Ariana Pia. "Investigating mitochondrial dysfunction in the nervous system." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/investigating-mitochondrial-dysfunction-in-the-nervous-system(b6c57b21-dfbb-4cf7-9833-269c8ef15368).html.
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Mitochondria play critical roles in the generation of cellular energy, apoptosis, calcium buffering, and mitochondrial dysfunction is strongly implicated in common neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. However, we still have a very poor understanding of the consequences of mitochondrial dysfunction in neurons in vivo. This thesis investigates mitochondrial dysfunction in patients with neurodegenerative disease and in a novel Drosophila model of neuronal mitochondrial dysfunction. I found that a single nucleotide polymorphism (SNP) in the gene mitochondrial transcription factor A (TFAM, SNP rs2306604 A > G) is associated with Parkinson’s disease dementia (PDD), but not with dementia with Lewy bodies (DLB). I have shown that mitochondrial DNA levels are significantly reduced in the frontal cortex of PDD patients, compared to controls. Furthermore, I have characterised the expression of TFAM and representative components of the mitochondrial electron transport (ETC) chain at the protein level in patients with Parkinson’s disease with and without dementia to determine whether rs2306604 A > G affects TFAM or ETC protein expression. In order to investigate mitochondrial dysfunction in a genetically tractable model system I have used a novel model of neuronal-specific mitochondrial dysfunction in Drosophila. I have used overexpression of TFAM, or expression of a mitochondrially-targeted restriction enzyme mitoXhoI, to cause mitochondrial dysfunction specifically in neurons. I have analysed the changes in mitochondrial DNA and mitochondrial gene expression in this model as well as characterising the behavioural and synaptic phenotypes. Using this model I performed microarray analysis to characterise the mitochondrial retrograde response in the Drosophila nervous system. This analysis revealed that neuronal mitochondrial dysfunction alters the expression of over 300 genes. I have validated the changes in expression of several of these genes in vivo. I have also characterised the involvement of the transcription factor hypoxia inducible factor alpha (HIFα) in the mitochondrial retrograde response in Drosophila. I found that HIFα regulates the expression of several retrograde response genes and that modulation of HIFα expression ameliorates some of the phenotypes associated with mitochondrial dysfunction.
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Poland, Stephen D. "Central nervous system infection with human cytomegalovirus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21311.pdf.
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Higgins, M. "Investigating ion channels of the nervous system." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604038.
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In this thesis, I present data concerning several stages in synaptic transmission. I have investigated some of the channel proteins involved in the initiation and the propagation of changes of membrane potential in nerve cells. I have also studied the process of clathrin mediated endocytosis, which is essential in the propagation of messages across the synapses between cells. Firstly, the Shaker voltage-gated potassium channel has been expressed using the baculovirus-mediated expression system. The expressed protein binds to charybdotoxin. The expression of correctly folded protein was increased by calnexin co-expression, or by using a 'weaker' baculovirus promoter. The protein has been purified using a Ni2+-NTA column and consists of tetrameric particles when analysed by electron microscopy and image processing. The cyclic nucleotide-gated channel has been purified from bovine retina and studied by image processing and electron microscopy to yield a 35Å-resolution model. This shows a large domain, which I propose to be the membrane-spanning domain. Attached to this are two smaller domains. I suggest that these are the cyclic nucleotide-binding domains and that they hang below the channel in the cytosol where they act as an independently functioning pair of dimers. Preliminary expression and purification of the α-subunit of the olfactory CNG channel suggests that similar analyses of this protein will soon be possible. Finally, the role of AP180 and AP2 in the formation of clathrin coated vesicles has been investigated.
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Painter, Michio Wendell. "Regeneration in the aging peripheral nervous system." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11422.
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In the peripheral nervous system (PNS), aging is associated with a number of disorders, including a decline in regenerative capacity after injury. Although this decline has been observed in both rodents and humans for decades, the cellular and molecular underpinnings of this defect have remained elusive. As such, the goal of this thesis was to elucidate, at least in part, how aging impinges on axonal regeneration.
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Harty, Helen Rosemary. "Nervous control of the sheep lymphatic system." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335493.
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Gordon, Tessa. "The peripheral nervous system : injury and disease." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6822/.
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Poor functional outcomes are frequent after peripheral nerve injuries despite the regenerative support of Schwann cells. Whilst motoneurons and to a lesser extent, sensory neurons survive the injuries, outgrowth of axons across the injury site is slow and the neuronal regenerative capacity is progressively reduced when neurons remain without targets and chronically denervated Schwann cells fail to support axon growth. Strategies including brief low frequency electrical stimulation that accelerates axon outgrowth and, in turn, target reinnervation and functional recovery, have excellent potential for translation to human patients. Other strategies including the insertion of cross-bridges between a donor nerve and a recipient denervated nerve stump, are effective in promoting functional outcomes after complete injuries. During muscle reinnervation the properties of the motoneurons and muscle fibers that they supply are rematched that provide some control of muscle force even when regenerating axons are misdirected to foreign targets. Axon sprouting from intact nerves is effective, although limited, in reinnervating denervated muscle fibers after incomplete injuries and in poliomyelitis. Studies in mouse models of amyotrophic lateral sclerosis however, indicate that sprouting is very limited with rapid and preferential loss of the largest and fastest contracting motor units during the asymptomatic phase of the disease.
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Bernick, Kristin Briana. "Cell biomechanics of the central nervous system." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67202.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2011.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 133-153).
Traumatic brain injury (TBI) is a significant cause of death and morbidity in both the civilian and military populations. The major causes of TBI, such as motor vehicle accidents, falls, sports concussions, and ballistic and explosive blast threats for military personnel, are well established and extensively characterized; however, there remains much to be learned about the specific mechanisms of damage leading to brain injury, especially at the cellular level. In order to understand how cells of the central nervous system (CNS) respond to mechanical insults and stimuli, a combined modeling/experimental approach was adopted. A computational framework was developed to accurately model how cells deform under various macroscopically imposed loading conditions. In addition, in vitro (cell culture) models were established to investigate damage responses to biologically relevant mechanical insults. In order to develop computational models of cell response to mechanical loading, it is essential to have accurate material properties for all cells of interest. In this work, the mechanical responses of neurons and astrocytes were quantified using atomic force microscopy (AFM) at three different loading rates and under relaxation to enable characterization of both the elastic and viscous components of the cell response. AFM data were used to calibrate an eight-parameter rheological model implemented in the framework of a commercial finite element package (Abaqus). Model parameters fit to the measured responses of neurons and astrocytes provide a quantitative measure of homogenized nonlinear viscoelastic properties for each cell type. In order to ensure that the measured responses could be considered representative of cell populations in their physiological environment, cells were also grown and tested on substrates of various stiffness, with the softest substrate mimicking the stiffness of brain tissue. Results of this study showed both the morphology and measured force response of astrocytes to be significantly affected by the stiffness of their substrate, with cells becoming increasingly rounded on soft substrates. Results of simulations suggested that changes in cell morphology were able to account for the observed changes in AFM force response, without significant changes to the cell material properties. In contrast, no significant changes in cell morphology were observed for neurons. These results highlight the importance of growing cells in a biologically relevant environment when studying mechanically mediated responses, such as TBI. To address this requirement, we developed two model systems with CNS cells grown in soft, 3D gels to investigate damage arising from dynamic compressive loading and from a shock pressure wave. These damage protocols, coupled with the single cell computational models, provide a new tool set for characterizing damage mechanisms in CNS cells and for studying TBI in highly controllable in vitro conditions.
by Kristin Briana Bernick.
Ph.D.
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Cadoux-Hudson, Thomas Anthony Daniel. "Nervous system metabolism : a magnetic resonance study." Thesis, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:88afc84d-c113-45c9-878a-b9dc99d84837.
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The aim of this thesis was to investigate the cellular biochemistry and metabolism of the human brain in vivo using magnetic resonance as the basic technique. Magnetic resonance imaging (MRI) can provide images of human structure and has already proved to be diagnostically useful in Neurology. Magnetic resonance spectroscopy (MRS) has the potential for measuring the tissue metabolite concentrations and metabolic rates of intracellular reactions in vivo. The great advantage of MRS is that many elements already present in abundance can be used to follow these intracellular reactions; no alien compounds need to be injected into the subject in the hope that they will eventually enter the tissue under investigation. However there are still considerable problems in receiving signal from the region of interest. No single approach in MRS has proved to be suitable for all investigations. An existing technique in MRS, phase modulated rotating frame imaging (PMRFI) was extended to measure absolute tissue concentration and enzyme flux rates of intracellular compounds containing phosphorus nuclei at above 1mmol/L tissue concentration in tissue volumes greater than 10ml. These technical limitations restricted the work of this thesis to the human cerebral hemispheres. Adenosine triphosphate (ATP) and phosphocreatine (PCr) are essential cytoplasmic compounds, providing energy for transport and biosynthetic pathways within the cell. Phosphorus MRS can also measure intracellular pH (pHi), providing an insight into ion metabolism within the cell. Finally 31P MRS can also measure the concentration of certain phospholipid groups and their precursors, phosphoethanolamine (PE) and phosphocholine (PC). The initial work carried out involved the construction, testing and modification of a probe suitable for clinical work. Studies were performed on subjects to establish a normal range for absolute tissue concentrations and enzyme flux rates through creatine phosphokinase. Studies on patients with primary brain tumours, acromegaly, herpes simplex encephalitis, HIV infections and those recovering following severe head injury were studied. Consistent changes in pHi, high energy phosphate and phospholipid metabolism were found in these conditions. The probable mechanisms underlying these changes are discussed and further investigations suggested.
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Coutinho, Maria Ester Freitas Barbosa Pereira. "Central nervous system autoimmunity in neuropsychiatric disorders." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3.
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The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment has hardly been considered. To study the relationship between maternal antibodies towards neuronal surface proteins and neurodevelopmental disorders in the foetus a dual approach was undertaken. First, pregnancy serum samples from mothers of children later diagnosed with a neurodevelopmental disorder and from mothers of children with typical development were screened for the presence of neuronal surface antibodies. Next, the effects of pathogenic neuronal surface antibodies in the offspring were assessed in a maternal-to-foetal transfer mouse model. Antibodies to neuronal surface proteins in the gestational serum, particularly CASPR2 antibodies, were found to associate with an increased risk of mental retardation and disorders of psychological development in the progeny. The animal model showed that mice exposed in utero to CASPR2 antibodies have long term behavioural sequelae and histological findings suggestive of abnormalities in brain development. These findings support a model in which maternal antibodies towards foetal neuronal proteins cause long-term behavioural deficits and permanent abnormalities at the cellular and synaptic level in a subset of children with neurodevelopmental disorders.
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Barnes, Jane Yvonne. "The autonomic nervous system and the heart." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21468.
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The mechanism by which the release of acetylcholine from cholinergic neurones in the heart is regulated are not well understood. A reliable and sensitive assay for acetylcholine is lacking. An HPLC method was also set up for the measurement of noradrenaline in coronary effluent samples from perfused, innervated rat hearts. The sensitivity was 0.5nM noradrenaline (inter-assay coefficient of variation, 4.9%). Four repeated left stellate ganglion stimulations (5 Hz, 60s, 0.8 mA), S1-S4, separated by a 15 min recovery period, demonstrated a progressive decline in noradrenaline overflow. The influence of duration of ganglion stimulation (30 or 60s) and coronary flow rate (5 or 10 ml g-1 min-1) on the noradrenaline overflow and functional response to four consecutive sympathetic ganglion stimulations, was examined. Baseline (pre-stimulation) mechanical performance of the preparation was stable. Lactate production was low and did not vary significantly between the groups. Stimulation induced changes in heart rate and left ventricular pressure were stable throughout the four stimulations (coronary flow rate 5 ml g-1 min-1). Noradrenaline overflow and contractility, however, showed a progressive decline from S1 to S4 (p<0.05). Reducing the stimulus duration from 60 to 30s delayed the onset of the decline in noradrenaline overflow and +dP/dt, while preventing the decline in the magnitude of the -dP/dt response. Increasing the coronary flow rate, completely prevented the decline in the response to nerve stimulation. In conclusion, vagal stimulation of the perfused, innervated rat heart results in marked negative inotropic and chronotropic changes, without detectable acetylcholine overflow. Repeated left stellate ganglion stimulation (S1-S4) results in reduced noradrenaline overflow and haemodynamic effects, that can be prevented using a coronary perfusion flow rate of 10 ml g-1 min-1. Left stellate ganglion stimulation does not confer a protective effect against ischaemia. Future studies of the role of the parasympathetic nervous system require more sensitive methods to detect acetylcholine.
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Hüppi, Petra Susan. "Serum antibodies to central nervous system antigens /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Cavanagh, Brenton. "Investigating Cell Proliferation in the Nervous System." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/370820.
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Cell proliferation is a strictly regulated process which is preceded by DNA synthesis and results in an increase in the number of new cells. It is essential for the development, regeneration and is upregulated in tumours. Whilst the study of cell proliferation is fundamental for many arms of biomedical investigation, the techniques used in its study have remained unchanged for decades. Neuroscience is one such field where cell proliferation in the adult can be a rare event and where molecular biology techniques are accelerating discoveries. Unfortunately, the limitations of studying cell proliferation have become a constraint in the field. This thesis examines the development of techniques to identify, characterise, quantify and profile proliferative cells in neural tissue. The techniques are provided in the context of a collection of studies that applied the techniques to secure data in a testable framework. The nervous system of the brain and olfactory mucosa were used to develop techniques to investigate cells on a histological and molecular scale. Initial investigation developed and improved tissue processing workflow and techniques to provide the optimal samples for histological analysis. The optical properties of the sample were improved, allowing deeper imaging in thick tissue sections. The embedding of frozen samples was altered to make use of gradients of OCT embedding media that minimised cell lysis. Embedment in the wax polyethelene glycol was used for sectioning at room temperature. Both techniques preserved tissue cytoarchitecture and antigenicity, allowing fluorescent labelling with multiple markers simultaneously in tissues with well conserved ultrastructure. These optimally prepared thick tissue samples provided a means of imaging multiple phenotypes and cell states in a single specimen (multiplexed), rather than multiple replicates of tissue sections, with different markers. The high optical clarity of the section facilitated high resolution 3D image acquisition, using optimised imaging techniques, further increasing the amount of information obtained from a sample set. These histological techniques were applied to the olfactory mucosa and substantia nigra to quantify cell proliferation and neurogenesis. EdU a thymidine analogue was used to label cells during the S-phase of the cell cycle, identifying cells that had undergone proliferation during exposure. It was shown that although neurogenesis was present in the olfactory mucosa, cell proliferation that occurred in the substantia nigra rarely gave rise to cells of a neural lineage. These techniques enabled the development of novel cell quantification methods, using stereology principles. Due to the ease and significantly less fragile nature, the substantia nigra as opposed to the olfactory system, was chosen to develop this technique. By quantifying subtypes of dopaminergic neurons in the substantia nira pars compacta of both the mouse and rat, an unbiased and accurate method of cell estimation was developed. The embedding method, multiple labelling immunofluorescence and serial optical sections obtained from thick specimens enabled significant improvements to stereological assessment. Thus, multiplexed cellular data was accurately quantified in brain tissue. These techniques were used to label multiple cell phenotypes during a defined period of exposure to EdU. This provided a powerful tool to investigate tissue where data on cell division and development was required together with cell – cell interaction of specific cell phenotypes that were labelled fluorescently. Specific tissue regions were quantified accurately and unbiasedly employing the advanced cell estimation technique. Expanding on the ability to effectively label and analyse cellular structures in tissue sections, in-situ, the capability to isolate and extract biomolecules from proliferating cells for analysis was developed. Thus, providing insight into the cellular differences that occur in proliferating cells. The basis of the technique involved the dissociation and fluorescent labelling of samples pre-labelled with EdU. These labelled cells were then isolated using FACS and RNA was then extracted for assessment of quality and analysis. The optimisation of each step was required to conserve the cell integrity and RNA quality. An enzyme cocktail that provided a gentle dissociation of neuronal tissue, decreased copper in the EdU labelling reaction, and minimising cell disruption during FACS was developed. Thereby, single proliferating cells and their RNA content was effectively extracted from neural tissues. The RNA extracted from the dividing cells showed significant expression differences of several key RNA products when compared to the non-dividing cells of the same tissue. These techniques provide a powerful tool kit to investigate proliferating cells of neural origin. Their use is not limited to the tissues and applications outlined in this thesis but are translatable to other tissue and biomolecules.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Stumpf, da Silva Taisa Regina. "Delivery Systems to Enhance Neural Regeneration in the Central Nervous System." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39391.
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Chan, Pok-man. "Cloning of hamster GAP-43 to study the expression and regulation of GAP-43 mRNA in the retina during degeneration and regeneration /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2063299X.
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Keary, Therese A. "Autonomic Nervous System Functioning in Posttraumatic Stress Disorder at Rest and During Stress: The Role of the Parasympathetic Nervous System." [Kent, Ohio] : Kent State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1219447142.
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Thesis (M.A.)--Kent State University, 2008.Title from PDF t.p. (viewed Oct. 15, 2009). Advisor: Joel Hughes. Keywords: PTSD, autonomic nervous system, parasympathetic nervous system, heart rate variability. Includes bibliographical references (p. 45-57).
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Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.
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Hannula, M. (Manne). "Information transmission capacity of the nervous system of the arm – an information and communication engineering approach to the brachial plexus function." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514272277.
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Abstract
The arm includes a large number of nerve fibres that transfer information between the central nervous system and the receptors, muscles and glands of the arm. In the nervous system there is continuous traffic. At rest, when only the receptors send information continuously towards the central nervous system, the traffic is not as intensive as during stress, e.g. during movements of the arm, when the central nervous system sends information towards the muscles, as well.
From an information and communication engineering perspective the nervous system of the arm is an information channel, the other end of which is in the central nervous system and the other end at the periphery of the arm. One principal question about such a communication system is what the maximum information transmission capacity of the channel is, e.g. how the information channel is dimensioned. The arm is a highly complex system with over sixty muscles moving it, and a huge number of sensory receptors in it. Nature has dimensioned the information channel of the arm to satisfy the requirements of the nervous system.
In this thesis a specific mathematical model is built in order to evaluate the maximum information transmission capacity of the nervous system of the arm. The model handles the nervous system of the arm as an entity in the light of information theory. The model uses the physiological and functional properties of the nervous system of the arm as the input and gives the estimate of the maximum information transmission capacity as the output.
The modelling yielded the result that the maximum information transmission capacity of the arm is about 10 Mbit/s. Hence, if a complete neural prosthesis of the arm were built, a single USB bus (12 Mbit/s) would suffice as a communication channel for each arm.
The mathematical model developed can also be applied to other parts of the peripheral nervous system. The aim of future research is to apply the developed model comprehensively to the human peripheral nervous system and to estimate the maximum information transmission capacity of the whole human peripheral nervous system.
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Biro, Andrew J. "Specific aspects of neurodegenerative disease." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28919.
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This thesis is broken into four chapters. The first two chapters summarize two separate lines of investigation into the role of a putative neurotoxin in the pathogenesis of Huntington's Disease (HD). The third chapter outlines an investigation of the putative role of beta-N-methylamino-L-alanine (BMAA) in the pathogenesis of amyotrophic lateral sclerosis (ALS), while the final chapter details a post-mortem investigation of the contents of biogenic amines and amino acids in the brain of a man who died of a familial form of parkinsonism.
Chapter I is a description of a chromatographic technique developed to isolate quinolinic acid (QA), an endogenous compound implicated in the pathogenesis of HD, from deproteinized human sera. A cation exchange column was used to selectively isolate QA, which was eluted with 10 mM HCl. The eluted fractions were analyzed by UV spectrometry to isolate and quantify QA. Once the fractions corresponding the elution of authentic QA were isolated, concentrated and the excess HCl removed, the fractions were added to growing fetal rat striatal explant cultures as an assay of neurotoxicity. Since HD involves the selective degeneration of GABAergic neurons in the striatum, the activity of glutamic acid decarboxylase, the final enzyme in the synthesis of GABA, was used to determine the viability of the cultures. Unfortunately, the method was confounded by the contamination of all effluents by compounds originating from the cation exchange
resin, which were discovered to be neurotoxic to the striatal cultures, and as a result the investigation had to be abandoned.
Chapter II describes an investigation designed to further characterize the nature of neurotoxicity observed in the sera obtained from patients with HD (Perry et al. 1987). Compounds with the capacity to selectively stimulate neurons at the N-methyl-D-aspartate (NMDA) receptor have been implicated in a variety of neurodegenerative disorders, including HD. Selective antagonists at the NMDA receptor have been shown to protect neurons from the degenerative effects of such "excitotoxins". The investigation described used MK-801, a potent noncompetitive
NMDA antagonist, in an attempt to protect fetal rat striatal cultures from the neurodegenerative effects of the sera obtained from HD patients. The results obtained were equivocal. No evidence was obtained to support a role of the NMDA receptor in the mediation of the neurotoxicity, and in addition the neurodegenerative effects of HD sera were not reproduced in the present investigation. A variety of possible explanations for the apparent discrepancy are suggested.
Chapter III describes an experiment intended to produce an animal model of ALS based on the observations by Spencer et al. 1987 that chronic oral administration of BMAA in monkeys produced the histological and behavioural characteristics of this disease. In the present investigation synthetic D,L-BMAA was given by gavage to mice over an eleven week period. Since BMAA is known to act at the NMDA receptor, a subset of the mice were also given MK-801 in an effort to protect them
from any deleterious effects based on the action of BMAA at this receptor. The animals were sacrificed at the end of the experiment, and biochemical analyses were performed on the striata and cortices of the animals. In addition, neuropathological studies were performed on the spinal cords, basal ganglia and related structures. The results indicated no biochemical or neuropathological abnormality as a result of BMAA administration.
Chapter IV describes a post-mortem investigation of a man who was a member of a well described pedigree which carries an autosomal dominant form of parkinsonism. The object of the investigation was to determine post-mortem levels of dopamine, noradrenaline, serotonin and their metabolites, in addition to amino acids in various regions of brain. Although conflicting evidence was obtained during life, neuropathological findings and the present neurochemical analyses confirm the degeneration of the nigrostriatal dopaminergic tract, characteristic of parkinsonism, in this man.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Johnson, Lise. "DECODING ELECTRIC FIELDS OF THE NERVOUS SYSTEM: INVESTIGATIONS OF INFORMATION STORAGE AND TRANSFER IN THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/193574.
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Electrical potentials are the fundamental currency of communication in the nervous system. The advanced executive functions of the prefrontal cortex and the motor commands delivered to the neuromuscular junction, though involved with very different aspects of behavior, both rely on time-varying electrical signals. It is possible to "listen to" the internal communications of the nervous system by measuring the electrical potentials in the extra-cellular space. However, this is only meaningful if there is some way to interpret these signals, which are incredibly complicated and information rich. This dissertation represents an attempt to decode some of these signals in order to reveal their significance for behavior and function. The first study is an investigation of the relationship between different elements of the local field potential in the prefrontal cortex and memory consolidation. It is shown that certain electrographic signatures of non-rapid eye movement sleep, namely K-complexes and low-voltage spindles, are correlated with neuronal replay of recent experiences. It is also shown that the global fluctuations of activity in the population of cells, known as up/down states, is correlated with neuronal replay. Finally, it is shown that high-voltage spindles are not correlated with memory replay, and are therefore functionally different from low-voltage spindles. The second study focuses on the relationship between movements of the upper limb and the coordinated neural control, as measured by the electromyogram (EMG), of the muscles generating that movement. We show that different probability-based models can be used to predict what the pattern of EMG in the different muscles will be for any given kinematic state of the hand. In the third study it is demonstrated that the kinematic output associated with a particular pattern of EMG can be reproduced with electrical stimulation. Thus, it is not only possible to understand the commands issued by the nervous system, it is also possible to issue commands by interfacing with the nervous system directly. Finally, the design for an experiment that would combine EMG prediction with translation of EMG into electrical stimulus patterns is presented. The objective of this study would be to use these methods to fully control the upper limb in a way that would be useful for a functional electrical stimulation-based neuroprosthetic for spinal cord injured patients.
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Buenger, Usha Rita. "Rat visual system neurons grow axons along peripheral nervous system grafts." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=64487.
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Piani, Daniela. "Immune-mediated cytotoxicity in the central nervous system /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10423.
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Lamvik, Kate K. "Central Nervous System Associations in Neurofibromatosis Type 1." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1179426618.
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Thesis (M.S.)--University of Cincinnati, 2007.Advisor: Dr. Elizabeth K. Schorry. Title from electronic thesis title page (viewed June 30, 2010). Includes abstract. Keywords: Neurofibromatosis type 1 (NF1); optic pathway glioma (OPG); central nervous system (CNS). Includes bibliographical references.
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Suzumura, Akio. "Microglia : Immunoregulatory cells in the central nervous system." Nagoya University School of Medicine, 2002. http://hdl.handle.net/2237/5375.
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Peaire, Amy. "Neurotoxicity and neuroinflammation in the enteric nervous system." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6331.
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The enteric nervous system (ENS) is the intrinsic nervous system of the gastrointestinal (GI) tract. Damage and degeneration of the ENS is a feature of some GI diseases, such as inflammatory bowel disease (IBD), and is associated with several other diseases including diabetes mellitis and Parkinson's disease. The overall goal of this thesis research was to identify specific classes of compounds capable of inducing ENS degeneration. These studies are intended to form a knowledge base upon which further studies can build towards the goal of preventing or attenuating clinical ENS damage. Reactive oxygen species (ROS), proinflammatory cytokines, and the process of anoxia-reoxygenation have been identified as inducers of CNS neurodegeneration and mediators in the neuropathogenesis of inflammatory diseases. As the ENS bears a considerable functional resemblance to the CNS, these compounds and processes are likely to have similar actions in this nervous system. Many of these mediators have been implicated in the pathogenesis of inflammatory diseases of the bowel, whereas initial studies of some of these mediators suggest their involvement in ENS neuropathogenesis. Thus, the general hypothesis of this thesis is that anoxia-reoxygenation, ROS, and the proinflammatory cytokine tumor necrosis factor-alpha (TNF) act on the ENS to induce neurodegeneration. In summary, the findings of this thesis are consistent with the hypothesis that inflammatory mediators can induce enteric neurodegeneration. This study identified specific inflammatory mediators as inducers of enteric neurodegeneration, characterized their neurodegenerative properties, and identified GDNF as a neuroprotective agent. Subsequent investigations further defined the respective roles of inflammatory immunocytes and the pro-inflammatory cytokine TNF in enteric neuronal cell death relevant to IBD pathogenesis. These findings are intended to form a basis for further studies into the mechanisms underlying clinical enteric neurodegeneration in disease pathogenesis. (Abstract shortened by UMI.)
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Armstrong, Rachel G. "Autonomic nervous system function following exercise-induced hyperthermia." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28362.
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Exercise in the heat is associated with cardiovascular and thermoregulatory disturbances that can persist postexercise. The effect of orthostasis on autonomic nervous system function following exercise-induced hyperthermia (EIH) remains to date unclear. Insight into the mechanisms of control is beneficial to those encountering orthostatic challenges after activity-induced hyperthermia.
We evaluated the short-term postexercise cardiovascular and thermoregulatory responses to repeated orthostatic challenges performed in a hyperthermic state and the effects of EIH on autonomic nervous system function during repeated orthostatic challenges in the early and late-stages of recovery.
We conclude that following EIH, the cardiovascular system maintained arterial pressure and cardiac output during repeated 70° head-up tilts. Nonthermal baroreceptor control predominates over thermal control of cutaneous vascular conductance during postural challenges following EIH, but no effect was observed in local sweat rate. The short-term reductions in baroreceptor sensitivity and heart rate variability following EIH were re-established following a 24-h recovery period.
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Lee, Yong Beom. "Cytokine network in the human central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ38925.pdf.
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Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.
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Beckers, Patrick [Verfasser]. "Nemertean nervous system : a comparative analysis / Patrick Beckers." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1044081511/34.
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Jackson, Johanna Sara. "Stem cell tracking in the central nervous system." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446551.
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