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1
Cina, Cima. "Distribution of locomotor-labelled neurons in the neonatal rat thoracolumbar spinal cord." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23253.pdf.
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Jones, Philip Leslie St John. "Structure-activity studies of novel compounds acting at metabotropic excitatory amino acid receptors in neonatal rat spinal motoneurons." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385687.
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Richard, Levine, Richard Vaillancourt, and Ralph Fregosi. "Evaluation of the Brainstem Spinal Cord Preparation in the Neonatal Rat as a Model for Prenatal Nicotine Exposure." The University of Arizona, 2012. http://hdl.handle.net/10150/614504.
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Class of 2012 AbstractSpecific Aims: The goal of this project was to evaluate the use of a preparation of the brainstem and spinal cord of neonatal rats that has been widely used for observing and quantifying central nervous activity, as well as the response to pharmacological manipulation. To achieve this, we specifically aimed to remove the intact brainstem and spinal cord of newborn rats, and develop a preparation that would maintain physiological function and allow for recording of electrical activity. Methods: Multiple dissections were performed on neonatal rats. Conditions during the dissections were controlled to maintain physiological function. Once removed, the intact brainstem and spinal cord was placed in a preparation that allowed for manipulation and access to nerve rootlets. Finally, glass suction electrodes were used to record electrical activity directly from the nerve rootlets. Once recorded, the data were stored on a hard drive for further analysis. Main Results: We were successful in isolating the intact brainstem and spinal cord in neonatal rats while maintaining physiological conditions and nervous activity. The preparation allowed for easy access to nerve roots as well as customization for different experiments. We were also successful in recording nerve activity in the preparation and collection of data for use in future experiments Conclusions: We conclude that the brainstem spinal cord preparation described in this study is a valuable tool that allows for recording and analysis of nerve activity, and specifically for measurement of respiratory motor output. This is a preparation that can be used in a variety of experiments that attempt to observe or quantify the activity of central nerve cells and allows for pharmacological interventions that could be applied in various experiments.
4
Hase, Takao. "Locomotor performance of the rat after neonatal repairing of spinal cord injuries : Quantitative assessment and electromyographic study." Kyoto University, 2002. http://hdl.handle.net/2433/149710.
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Levine, Richard. "Evaluation of the Brainstem Spinal Cord Preparation in the Neonatal Rat as a Model for Prenatal Nicotine Exposure." The University of Arizona, 2012. http://hdl.handle.net/10150/623649.
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Class of 2012 AbstractSpecific Aims: The goal of this project was to evaluate the use of a preparation of the brainstem and spinal cord of neonatal rats that has been widely used for observing and quantifying central nervous activity, as well as the response to pharmacological manipulation. To achieve this, we specifically aimed to remove the intact brainstem and spinal cord of newborn rats, and develop a preparation that would maintain physiological function and allow for recording of electrical activity. Methods: Multiple dissections were performed on neonatal rats. Conditions during the dissections were controlled to maintain physiological function. Once removed, the intact brainstem and spinal cord was placed in a preparation that allowed for manipulation and access to nerve rootlets. Finally, glass suction electrodes were used to record electrical activity directly from the nerve rootlets. Once recorded, the data were stored on a hard drive for further analysis. Main Results: We were successful in isolating the intact brainstem and spinal cord in neonatal rats while maintaining physiological conditions and nervous activity. The preparation allowed for easy access to nerve roots as well as customization for different experiments. We were also successful in recording nerve activity in the preparation and collection of data for use in future experiments Conclusions: We conclude that the brainstem spinal cord preparation described in this study is a valuable tool that allows for recording and analysis of nerve activity, and specifically for measurement of respiratory motor output. This is a preparation that can be used in a variety of experiments that attempt to observe or quantify the activity of central nerve cells and allows for pharmacological interventions that could be applied in various experiments.
6
Miller, Jacqueline Chantal. "Pharmacological characterisation and the immunohistochemical localisation of glutamate receptor subtypes in the lumbar region of the neonatal rat spinal cord." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247861.
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More, Julia Carrie-Ann. "Pharmacological characterisation of kainate receptors in the neonatal rat spinal cord using novel antagonists based on the natural product willardine." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396711.
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Plenderleith, M. B. "The effects of neonatal capsaicin treatment on the functional properties of sensory neurones in the dorsal horn of the rat spinal cord." Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356742.
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Altas, Melanie. "Spinal cord transplants in a rat model of spinal cord injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/MQ49305.pdf.
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Krenz, Natalie. "Plasticity in the rat spinal cord following spinal cord transection, contribution to autonomic dysreflexia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0008/NQ40268.pdf.
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Stavridis, Stavros I. "Characterization of postnatal rat spinal cord slice cultures and studies on co-cultures of postnatal rat spinal cord and motorcortex /." Frankfurt a.M, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254590.
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Gibson, Claire. "Interactions between afferent pathways in spinal cord development." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311132.
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Li, Ying. "Axon growth in the adult rat spinal cord." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308967.
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Kumar, David Vijay. "Glycine receptors in the developing rat spinal cord." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/289778.
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Inhibitory glycine receptors (GlyRs) undergo developmental regulation with α2 subunits most abundant at prenatal and early postnatal stages, and α1 subunits predominating in adults. In comparing the relative amounts of mRNA for two known splice variants of the α2 subunit, α2A and α2b, in the rat spinal cord at different stages of development, I found evidence for the existence of an additional, novel variant. This variant, missing exon 3, I have termed "α2N." Examination of the RNA from spinal cords of different-aged rats indicated that α2N undergoes dramatic down-regulation during prenatal development. Its mRNA forms a significant portion of the α2 subunit pool at E14, but is nearly undetectable at the time of birth. I also examined the developmental changes in two factors that can regulate GlyR α2 pre-mRNA splicing, the splicing factor neurooncological ventral antigen-1 (Nova-1) and the brain isoform of the polypyrimidine tract binding protein (brPTB). Treatment of neurons in culture with antisense oligonucleotides to "knock down" one of the Nova-1 variants altered the expression of GlyR α2N. These results suggest that the relative levels of the variants of Nova-1 and brPTB may play a role in the developmental regulation of GlyR α2N. Based on these results I propose a model for the developmental regulation of GlyR α2N. These results provide evidence for a novel splice variant of the GlyR α2 subunit that undergoes dramatic developmental regulation, and reveal the developmental profiles of two possible regulators of its expression during development.
15
Hoy, Kevin Corcoran. "AMPA-receptor mediated plasticity within the rat spinal cord." [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-3056.
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Gensel, John Carib. "Modeling and treatment of rat cervical spinal cord injury." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1167753874.
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Clatworthy, A. L. "Modulation of nociceptive processing in the rat spinal cord." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382589.
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Jennings, Ernest Albert. "Cutaneous afferent evoked activity in the postnatal rat spinal cord." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369052.
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Karam, S. M. "Morphine modulation of excitatory transmission in the rat spinal cord." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444763/.
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The transmission of painful messages from the periphery involves complex interactions between excitatory and inhibitory neurotransmitter systems in the spinal dorsal horn. The balance between these receptor events determines the level of pain transmission. Within the spinal cord, neuronal sensitization plays a key role in altering the ascending messages to the brain. Morphine, widely used in pain control, acts on inhibitory mu opioid receptors located both on small diameter primary afferent fibres and postsynaptic sites. The aim of my studies was to determine how various excitatory transmitter systems at spinal levels are modulated by morphine in rats. The activation of the receptor for substance P, the NK-1 receptor, and the NMDA receptor for glutamate, on dorsal horn neurons are thought to contribute to wind-up pain and central sensitisation underlying a number of abnormal clinical pain states. Using in vivo electrophysiological studies and behavioural measures, I have studied the relations between peripheral inputs and central sensitisation using NK-1 and NMDA receptor agonists and further used a surgical neuropathic model and investigated the actions of morphine on the neuronal activity and pain behaviours. I have also investigated NMDA receptors located on peripheral endings of sensory nerves, and found a lack of functional effects of these receptors in pathophysiological states. Finally, the role of the excitatory 5HT3 receptor was assessed using the antagonist ondansetron in the neuropathic pain model, as was the combination of morphine and ondansetron which was more effective in inhibiting some of the pain behaviour seen in neuropathic pain than ondansetron alone. The actions of morphine, at a non-sedating dose, could overcome central sensitisation, the actions of ondansetron confirm the role of descending facilitations after nerve injury and the results demonstrate how the balance between excitation and inhibition can alter the level of pain and its control.
20
Vu, Hung. "Mechanisms of rapid receptive field reorganization in rat spinal cord." Thesis, University of North Texas, 2002. https://digital.library.unt.edu/ark:/67531/metadc3197/.
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Rapid receptive field (RF) reorganization of somatosensory neurons in the rat dorsal horn was examined using extracellular single unit recording. Subcutaneous injection of lidocaine into RFs of dorsal horn neurons results in expansion of their RFs within minutes. The expanded RFs appear adjacent to or/and proximal to original RFs. Out of 63 neurons tested, 36 (58%) show RF reorganization. The data suggest that dorsal horn of spinal cord is one of the initial sites for RF reorganization. The neural mechanisms of this effect are not well understood. We propose that changes in biophysical properties (membrane conductance, length constant) of the neurons resulting from lidocaine injection contribute to RF reorganization. Iontophoretic application of glutamate onto dorsal horn neurons that show lidocaine induced RF's expansion were used to test the model. Application of glutamate produced reduction of reorganized RFs in 9 of 20 (45%) tested cells. Application of NBQX produced no effect on either original or expanded RFs indicate that RF shrinkage effects of glutamate involve NMDA receptors. The results are consistent with the prediction of the proposed model. Subcutaneous injection of capsaicin into tactile RFs of low threshold mechanoreceptive dorsal horn neurons produced no effect on the RF sizes that are consistent with other studies. Following the injection, the original RFs were completely silenced (46%) or remained responsive (54%).
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Boxall, Sarah Jane. "Contribution of metabotropic glutamate receptors to spinal nociceptive transmission in the rat spinal cord." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268057.
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Lucas, Erin. "Measuring in vivo internal spinal cord deformations during experimental spinal cord injury using a rat model, radiography, and fiducial markers." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27808.
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Spinal cord injuries (SCIs) are commonly studied experimentally by causing injury to rodent spinal cords in vivo and analyzing behavioral and histological results post injury. Few researchers have directly investigated the deformation of the in vivo spinal cord during impact, which is thought to be a predictor of injury. This knowledge would help to establish correlations among impact parameters, internal structure deformation, and histological and functional outcomes. The objective of this thesis was to develop a radiographic method of tracking the real-time internal deformations of an anesthetized rat‘s spinal cord during a typical experimental SCI.
A technique was developed for injecting fiducial markers into the dorsal and ventral white and grey matter of in vivo rat spinal cords. Two radio-opaque beads were injected into C5/6 in the approximate location of the dorsal and ventral white matter. Four additional beads were glued to the surface of the cord caudal and cranial to the injection site (one dorsal, one ventral). Overall bead displacement was measured during quasi-static compression using standard medical x-ray equipment. Dynamic bead displacement was tracked during a dorsal impact (130mm/s, 1mm depth) by imaging laterally at 3,000 fps using a custom high-speed x-ray system.
The internal spinal cord beads displaced 1.02-1.7 times more than the surface beads in the cranial direction and 2.5-11 times more in the ventral direction for the dynamic impact and maximum quasi-static compressions. The dorsal spinal cord beads (internal and surface) displaced more than the ventral spinal cord beads during all compressions. Finite element modeling and experimental measurements suggested that bead migration with respect to the spinal cord tissue was small and mostly insignificant.
These results support the merit of this technique for measuring in vivo spinal cord deformation. The differences in bead displacements imply that the spinal cord undergoes complex internal and surface deformations during impact. Many applications of this technique are conceivable including validating finite element and surrogate models of the spinal cord, comparing localized grey and white matter motion during impact to histological findings, and improving SCI preventative and treatment measures.
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Tiong, Sheena Yin Xin. "Characterisation of interneurons in lamina II of the rat spinal cord." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2699/.
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Lamina II of the dorsal horn contains numerous small neurons with varying morphologies, most of which have axons that remain within the spinal cord. It can be distinguished from the other laminae by its lack of myelinated fibres and its constituent interneurons that are densely packed. This region is the major termination site for unmyelinated (C) primary afferent fibres, which convey mostly nociceptive information. It also receives inputs from thinly myelinated (Aδ) fibres, some of which are nociceptive. In spite of its importance and several past attempts, little is known of its neuronal circuitry. This is mainly due to the great functional and morphological diversity of lamina II interneurons, which has made characterisation difficult. A comprehensive classification scheme is essential to identify discrete functional populations of lamina II interneurons, and to enable understanding of their roles in the local neuronal circuitry. The present study aims to investigate the physiological, pharmacological and morphological properties of lamina II interneurons recorded in an in vitro slice preparation from adult rat spinal cord. These properties were correlated with the neurotransmitter content of each cell, which was identified by detection of vesicular transporters in axonal boutons, in order to distinguish discrete functional subpopulations of cells in this region. Both inhibitory and excitatory interneurons were identified in lamina II, based on their expression of vesicular GABA transporter (VGAT) or vesicular glutamate transporter (VGLUT2), respectively. None of the cells that had VGAT-immunoreactive axons displayed staining for VGLUT2, and vice-versa. Injection of depolarising current evoked tonic-, transient-, delayed-, gap-, reluctant- and single spike-firing among these cells. Discharge pattern was strongly related to neurotransmitter phenotype, since most excitatory cells, but very few inhibitory cells had firing patterns that could be attributed to A-type potassium (IA) currents (i.e. delayed, gap or reluctant-firing). This suggests that excitatory lamina II interneurons with IA –type firing patterns are involved in plasticity that contributes to pain states. The majority of inhibitory cells displayed tonic-firing pattern in response to depolarisation. There was also an obvious difference in the response of lamina II neurons to hyperpolarisation, since the majority of inhibitory cells showed inward currents while most excitatory cells displayed transient outward currents. Noradrenaline and serotonin hyperpolarised both inhibitory and excitatory neurons, while only inhibitory neurons responded to somatostatin. This is consistent with the findings of a previous study that had shown that the somatostatin 2 receptor (sst2a) is only expressed by inhibitory neurons in lamina II, and suggests that the pro-nociceptive effects of somatostatin are mediated by ‘disinhibition’. The somatodendritic morphology of 61 lamina II interneurons was reconstructed from projected confocal images of Neurobiotin labelling and assessed according to the morphological scheme developed by Grudt and Perl (2002). Although cells in the islet, central, vertical and radial class were identified, a substantial number of cells (19/61) had morphology that was atypical or intermediate between two classes and therefore could not be classified. Certain morphological types were consistently found in the inhibitory or excitatory population: all islet cells were GABAergic, while all radial cells and most vertical cells were glutamatergic. However, the correlation between these properties may be complex, since there was a considerable diversity in the remaining cells. Some glutamatergic interneurons had axons that contained somatostatin and many of these also contained enkephalin. Somatostatin-expressing glutamatergic cells included various morphological types, while enkephalin was detected in the axons of vertical and radial cells. All cells with axons that were somatostatin- and enkephalin-immunoreactive had delayed-firing patterns. Taken together with the pharmacological data from the present study, this suggests that somatostatin released from these glutamatergic neurons would hyperpolarise subsets of inhibitory neurons and causes disinhibition. This could lead to alterations of pain thresholds. The results from this study demonstrate that distinctive populations of inhibitory and excitatory interneurons can be recognised in lamina II, and these cells are most likely to correspond to discrete functional groups. Electrophysiological, neurochemical, morphological and pharmacological properties of neurons can be correlated but this is likely to be very complex. Future investigations that combine various approaches should allow further understanding of the specific roles of lamina II interneurons in nociceptive processing within the spinal cord.
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Du, Beau Amy. "Neurotransmitter phenotypes of descending systems in the rat lumbar spinal cord." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4721/.
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Sensorimotor processes within the spinal cord are profoundly influenced by descending systems from the brain yet the neurotransmitter phenotypes of these systems remains enigmatic. Using tract tracing methods, this study identifies the neurochemical content of axons descending from the sensorimotor cortex and sites within the anatomically diverse reticular formation. There are several classes of neurons in spinal lumbar segments targeted by these descending systems which contribute to recruiting adaptively appropriate motor patterns. This study investigates the neuronal targets of descending systems and the neurochemical content of their inputs. Immunofluorescent tissue containing labelled neuronal processes were examined and reconstructed interneurons were defined according to their neuronal geometry and morphology across laminar boundaries.
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Zhang, Li Ping. "Investigations of C-FOS expression in rat spinal cord in vitro." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242708.
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Cholas, Rahmatullah H. (Rahmatullah Hujjat). "Collagen implants to promote regeneration of the adult rat spinal cord." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/35658.
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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2006.Includes bibliographical references (leaves 50-52).
Over 250,000 people in the United States currently live with a spinal cord injury and approximately 11,000 new cases occur every year. People with spinal cord injuries experience a significant reduction in quality of life due to the many problems that arise from damage to the spinal cord including paralysis and loss of sensation below the location of injury, loss of bowel and bladder function, loss of sexual function, and impaired respiration. Despite considerable ongoing research in the area of nerve regeneration by various institutions, satisfactory treatment for spinal cord injury has not yet been discovered. Previous studies have had considerable success in facilitating the regeneration of severed peripheral nerves through the use of collagen based implants used to bridge the resulting gap between the severed nerve stumps. The current study aims to apply this same regenerative approach to a defect created in the spinal cord of adult rats. The objective is to evaluate the efficacy of three different collagen implants toward the regeneration of the spinal cord. The experimental spinal cord injury was a complete transection at T7 and T9 and the removal of the spinal cord segment between the two transections, creating a 5 mm gap.
(cont.) This study contained four experimental groups. Group I was the control group. The animals in this group had a complete spinal cord transection as described above but received no implantation. Group II received a resorbable dura replacement sheet of collagen, 1 mm thick, cut from the BioGide(® membrane which was placed extradurally over the dorsal aspect of the wound site. Group III used the BioGide® membrane as a wrap which bridged the gap between the two cord stumps. Group IV used a collagen tube, fabricated using a freeze-drying process, to bridge the gap. Histological analysis at 6 weeks after implantation showed Groups III and IV to have more longitudinally oriented reparative tissue filling the defect area as well as fewer fluid-filled cysts. Quantitative analysis of axonal regeneration showed the collagen implants to be supportive of the regeneration of axons into the center of the defect.
by Rahmatullah H. Cholas.
S.M.
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Horiuchi, Ricardo Shiniti Oka. "Analise proteomica da região lombar da medula espinhal de ratos durante o periodo pós-natal." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314371.
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Orientador: Jose Camillo NovelloDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Conhecer os mecanismos que regem a embriogenese e a maturacao do sistema nervoso e de grande interesse para todos os diferentes ramos da neurociencia. Durante o desenvolvimento dos mamiferos sabe-se que ocorrem fenomenos que levam a definicao do numero de neuronios e refinamento das conexoes sinapticas, que tem caracteristicas proprias nas diferentes regioes do sistema nervoso e podem diferir tambem quanto a sua duracao. Apos o nascimento, diversos sinais neurais e bioquimicos podem modificar significativamente a organizacao morfologica e funcional dos circuitos da medula espinhal, periodo que podemos considerar como critico. Tendo em vista esses fatores, o trabalho visou analisar o proteoma, complemento proteico completo do genoma, da regiao lombar da medula espinhal de rato em busca de proteinas envolvidas com o processo de neurodesenvolvimento. Amostras de medula de rato foram coletadas em diferentes tempos de vida, abrangendo o dia do nascimento (P0), com dois (P2), quatro (P4), sete (P7) e vinte e um (P21) dias de vida e comparadas utilizando-se a eletroforese de duas dimensoes em gel de poliacrilamida e identificacao por espectrometrias de massas. Os perfis proteomicos obtidos permitiram identificar proteinas diferencialmente expressas entre as amostras de P4 e P21. Destas, cinco foram mais expressas em amostras de P4: XLas, fragmento da cadeia beta da ATP sintase trasnportadora de H+, a cadeia 2B da tubulina beta e a neuromodulina; e tres foram mais expressas nas amostras de P21: GFAP, neurofilamento de cadeias polipeptidicas leve e reguladora da proteina G. Estes resultados indicam que ha uma expressao proteica diferencial e que sao as provaveis proteinas envolvidas no processo de desenvolvimento pos-natal da medula espinhal.
Abstract: To know the mechanisms that govern the embryogenesis and the maturing of the nervous system is of great interest for all the different branches of the neuroscience. During the development of the mammals one is known to take place phenomena that lead to the definition of the number of neurons and refinement of the synaptic connections, which has characteristics own in the different regions of the nervous system and which duration can also differ as for his duration. After the birth, several neurons signs and biochemical can modify significantly the morphological and functional organization of the circuits of the spinal cord, period that we can consider like critic. In mind these factors, the work aimed to analyses the proteome, the genome complete protein complement, of the lumbar region of the spinal cord of rat in search of proteins wrapped with the process of neurodevelopment. Samples of rat's spinal cord were collected in different times of life, including the day of the birth (P0), with two (P2), four (P4), seven (P7) and twenty one (P21) days of life and compared by two dimensional gel electrophoresis and identification by mass spectrometry. The proteomics profiles obtained allowed to identify proteins differently expressed between the samples of P4 and P21. Of this, five were more expressed in samples of P4: XLas, H+ transporting ATP synthase beta chain (fragment), Tubulin beta-2B chain and the neuromodulin; and three were more expressed in the samples of P21: GFAP, Neurofilament light polypeptide and Regulator of G-protein signaling 14. These results indicate that there is a differential protein expression and which are the probable proteins wrapped in the process of native-powders development of the spinal cord.
Mestrado
Bioquimica
Mestre em Biologia Funcional e Molecular
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Crowley, Kristine C. "Neurochemical substrates of locomotor and non-locomotor rhythms in rat spinal cord." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ31972.pdf.
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Gardner, E. "Factors influencing gene expression in the rat spinal cord following noxious stimulation." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599312.
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Noxious stimulation increases the levels of AP-1 and other immediate early gene (IEG) proteins in the spinal cord. These transcription enhancers regulate the expression of a second set of genes which have the potential to cause long-term changes in neuronal phenotype and function. In the spinal cord, such changes are manifested as hypersensitivity to stimulation leading to chronic pain states. One putative target of IEG control is the gene encoding the opioid peptide dynorphin. Robust increases in this gene are seen in the spinal cord in animal models of pain and its presence has been correlated with alteration of neuronal function. This study has used the rat formalin test as a model for gene activation in the spinal cord. The stimulus-specificity of changes in gene expression caused by hind-paw injection of dilute formalin was compared with similar injection of the neurotoxin capsaicin. The contribution of different neurotransmitters to the IEG response was assessed by pharmacological means in formalin-injected animals. Finally, the presence of functional IEG proteins in the spinal cord of formalin-injected animals was assessed by gel shift assay. Formalin and capsaicin produced different physiological and behavioural responses; formalin provoked long-lasting inflammation and prolonged biphasic nociceptive behaviour, whilst capsaicin was non-inflammatory and without a profound effect on behaviour. However, both treatments caused similar short-term upregulation in IEG expression in the spinal cord followed by an increase in preprodynorphin mRNA. Thus even brief noxious stimulation, as caused by capsaicin, was capable of significantly altering neuronal gene expression. Pharmacological investigation of the formalin test showed that both phases of the behavioural response could be selectively inhibited by non-NMDA and NMDA glutamate antagonists (NBQX and HA966).
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Teoh, Hwee. "Modulation of neurotransmitter amino acid release from the rat isolated spinal cord." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321647.
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Behrmann, Donald Lee. "Modelling of spinal cord injury in the rat : effects of pharmacologic intervention /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487777901658184.
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Boyce, Sheri Lynn. "Apoptosis of Oligodendrocytes and Microglia after Spinal Cord contusion in the Rat /." The Ohio State University, 1999. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488190595942167.
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Ward, R. A. "The interaction of substance P and 5-hydroxytryptamine in the spinal cord." Thesis, Bucks New University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376427.
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Puga, Denise Alejandra. "The opponent consequences of intermittent and continuous stimulation within the rat spinal cord." [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-1605.
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Mattucci, Stephen Frank Ernesto. "A biomechanical investigation of a dislocation spinal cord injury in a rat model." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/64175.
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Traumatic spinal cord injuries clinically occur in a heterogeneous fashion, including at different spinal levels, injury velocities, and injury mechanisms. Clinical treatment options, such as early surgical decompression produce inconsistent recovery outcomes in the patient population, despite demonstrating effectiveness in preclinical animal models. The most common biomechanical factors, such as cervical level, high-energy impact and dislocation injury mechanism, are not adequately represented in preclinical models, which may explain the lack of agreement between clinical studies. The overall objective of this thesis was to investigate the biomechanics of a high-speed cervical dislocation rat model at acute stages, refine the model, and incorporate residual compression. The temporal progression of acute SCI was investigated in different injury mechanisms, where dislocation injuries demonstrated the fastest loss of white matter tissue. To refine the dislocation model, new vertebral injury clamps were designed with a feature allowing the clamps to pivot and self-align when tightened. The vertebral kinematics during a dislocation injury were analysed using high-speed x-ray and clamp slippage was significantly reduced with the self-aligning clamps, compared to the existing clamps. This study also emphasized the importance of validating injury displacements against input parameters, particularly when comparing results or reproducing injuries. In order to implement residual compression within the dislocation model, injury parameters were independently investigated. Electrophysiology techniques were implemented to determine a minimum residual compression depth that affects signal conduction following a traumatic injury. Continuously holding the residual compression following the initial injury induced a significantly different physiological response compared to when the injury was immediately reduced. Behavioural outcome was used to identify severities following a range of displacements, and four hours of residual compression was survivable following a ‘mild’ traumatic injury, indicating suitable parameters for future studies. Rats of the same weight were identified to have different anatomical dimensions and structural properties of the spinal column, potentially influencing injury outcomes in closed-column models. The continued development and implementation of the cervical dislocation injury model in the rat will deepen understanding of SCI biomechanics and provide an additional clinically-relevant injury model for testing the robustness of potential treatment therapies.Applied Science, Faculty of
Graduate
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Euler, Mia von. "Experimental spinal cord injuries : a histopathological, neurological, and pharmacological study in the rat /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3461-4/.
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Seagrove, Lucinda Claire. "Characteristics, plasticity and pharmacology of Lamina I neurones in the rat spinal cord." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407176.
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Al-Izki, Sarah. "Actions of the rubrospinal tract in the cervical spinal cord of the rat." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445255/.
Full textAbstract:
This thesis describes the electrophysiological and anatomical distribution of the projections from the rubrospinal tract (RST) in the cervical spinal cord of the rat, in control animals and animals with a dorsal column lesion. It also describes the behavioural changes following the lesion. The RST originates from the magnocellular region of the red nucleus (RNm), from where its axons project to the contralateral spinal cord, mostly in the dorsolateral funiculus (DLF). Previous work has shown that the RST is implicated in precise limb movements. It has also been demonstrated that where the corticospinal tract (CST) is impaired, the RST is capable of motor control and will compensate for the damage to the CST. In terminal experiments, electrical stimulation of the RNm elicited two orthodromic descending volleys recorded from the contralateral DLF. The latency of the early one indicated that it is produced by direct activation of fibres in or close to the RNm. Temporal facilitation demonstrated that the second volley is elicited by synaptic excitation of RNm neurons. Postsynaptic responses related to the second volley were seen only in the intermediate zone of the contralateral spinal cord. In animals with a dorsal column lesion, the distribution of RST actions is similar to that of the controls. Functional recovery in lesioned animals was assessed using three behavioural tests: pellet retrieval, cylinder, and the sticker removal test. The cylinder and sticker removal tests have both shown to be ineffective in providing important information on the recovery. However, the pellet retrieval test, which requires skilled motor control, has enabled correlation of recovery to size of lesion. The results obtained demonstrate that lesion to dorsal columns alone has little effect on the success rate. The anatomical and electrophysiological experiments provide information on the distribution of RST actions, which will be correlated in the thesis with the behavioural results. Evidence for plasticity will be discussed.
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Abelson, Klas. "Acetylcholine in Spinal Pain Modulation : An in vivo Study in the Rat." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4834.
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Bufton, Hywel Rhys. "A pharmacological study of voltage-sensitive calcium channels, 5-hydroxytryptamine receptors and kainate receptors at the spinal level in the rat." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388015.
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Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Full textAbstract:
The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
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Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Full textAbstract:
Doctor of PhilosophyThe general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
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Sun, Fang. "Investigation of the stimuli inducing delayed oligodendrocyte apoptosis after rat spinal cord contusion injury." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148493870.
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Silva, Gabriel A. "Metabotropic glutamate receptor expression in rat spinal cord astrocytes in vitro and in situ." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0011/MQ29351.pdf.
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Gilron, Ian. "Effects of intravenous anaesthetics on formalin-induced FOS immunoreactivity in the rat spinal cord." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0004/MQ44172.pdf.
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Hilton, Kathryn Jane. "Modulation of preprotachykinin-A promoter activity using novel protocols in the rat spinal cord." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413201.
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Withers, Michelle Dawn. "Regulation of glycine receptors by embryonic rat spinal cord neurons during development in vitro." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187369.
Full textAbstract:
This work addresses developmental regulation of neurotransmitter receptors in the vertebrate central nervous system (CNS). Glycine receptors (GlyR) play a major role in inhibitory neurotransmission in the spinal cord. Changes in the types of GlyRs being expressed by embryonic rat spinal cord neurons are examined during development in vitro. Spinal cord neurons are cultured at the fourteenth day of gestation, prior to receiving afferent input. Previous work demonstrated a delayed expression of the adult-type GlyR α subunits. Reverse transcriptase-polymerase chain reaction demonstrates the presence of mRNA for GlyR α2 subunits by these neurons at early times in culture. The presence of GlyR α2 subunits are confirmed by immunofluorescence microscopy with a new α2 subunit specific antibody. These subunits appear by the first day in culture and exhibit a diffuse subcellular distribution. During the course of these experiments, populations of embryonic rats were found to differ in the subtypes of GlyR they expressed at early times during development. The expression of functional GlyRs is investigated in two populations of embryonic rats using whole-cell patch clamp recordings. The GlyR antagonist, strychnine, is used as a tool to distinguish between some forms of the GlyR. The two populations are similar in their onset of responsiveness to glycine and in the ion-dependence of the glycine-induced current. The strychnine-sensitivity of responses to glycine differs between the two populations. Neurons from the first population of rats exhibit a developmentally regulated increase in the sensitivity to strychnine, while the strychnine-sensitivity of responses to glycine by neurons from the second population remains high throughout development in culture. These results suggest that two populations differ in the type of functional GlyR they express during early development in culture. The relatively low sensitivity to strychnine exhibited during the first few days in culture by neurons from the first population of rats cannot be accounted for by changes in sensitivity to glycine or by non-specific cross-activation of γ-aminobutyric acid receptors (GABARs). Neurons from the first population undergo a gradual change from the predominant expression of a strychnine-insensitive GlyR to some form(s) of strychnine-sensitive GlyR.
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Mackie, Margaret. "The co-localisation and distribution of glutamate decarboxylase isoforms in the rat spinal cord." Thesis, University of Glasgow, 2006. http://theses.gla.ac.uk/9059/.
Full textAbstract:
GABA is one of the two main inhibitory neurotransmitters in the central nervous system, CNS (along with glycine, which has a major role in the brainstem and spinal cord). GABA regulates a number of functions in the CNS, and in the spinal cord, it is responsible for presynaptic inhibition of primary afferents and postsynaptic inhibition of neurons. GABA is produced by decarboxylation of L-glutamate by glutamate decarboxylase (GAD). Two GAD isoforms have been identified, GAD65 and GAD67. Antibodies raised against glutaraldehyde conjugates of GABA have been used to investigate the distribution of GABAergic cell bodies, whilst the distribution of GABAergic terminals has been examined with antibodies against GAD. Although GABAergic cell bodies are detected throughout the spinal grey matter, these are concentrated in laminae I-III of the spinal dorsal horn. GAD is present in axon terminals in all laminae of the rat spinal cord, but only a few immunoreactive cell bodies have been detected in the superficial dorsal horn. This differs from the situation in the brain, where many GAD-immunoreactive cell bodies can be found. Studies in the brain suggest that while most (if not all GABAergic neurons) synthesise both GAD isoforms, many have relatively high levels of one or other isoform. It is not known whether this is the case in the spinal cord. Until recently, most studies that have looked at the distribution of GAD have used antibodies that do not differentiate between the two isoforms, and such studies in the spinal cord have been qualitative and no attempt has been made to quantify GAD levels in individual laminae, or examine the co-localisation of GAD isoforms in individual boutons. The recent availability of antibodies that are directed against each isoform separately enables detailed studies to be performed that compare the distribution and co-localisation of the two isoforms, in this study, immunocytochemistry and confocal microscopy were used to examine the distribution and co-localisation of GAD65 and GAD67 in individual axonal boutons in each lamina of the rat spinal grey matter. The main finding of this part of the study was that although most GAD- immunoreactive boutons were labelled with both GAD65 and GAD67 antibodies, some showed similar intensities of both types of immunoreactivity whilst others appeared to have relatively higher levels of one or other of the GAD isoforms. This suggests that GAD-immunoreactive neurons are a heterogeneous population. Also, GAD-immunoreaetivity differed between each lamina of the spinal cord e.g. in the superficial dorsal horn, boutons that had relatively higher levels of either GAD65 or GAD67 were frequently found. In contrast, most boutons in the ventral horn displayed relatively high levels of GAD67, although discrete clusters of boutons that had high levels of GAD65 immunoreactivity were detected in lamina IX.
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Keefe, Kathleen Mary. "In Vivo Visualization of Neural Pathways in the Rat Spinal Cord Using Viral Tracing." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/521830.
Full textAbstract:
NeurosciencePh.D.
Much of our understanding of the fascinating complexity of neuronal circuits comes from anatomical tracing studies that use dyes or fluorescent markers to highlight pathways that run through the brain and spinal cord. Viral vectors have been utilized by many previous groups as tools to highlight pathways or deliver transgenes to neuronal populations to stimulate growth after injury. In a series of studies, we explore anterograde and retrograde tracing with viral vectors to trace spinal pathways and explore their contribution to behavior in a rodent model. In a separate study, we explore the effect of stimulating intrinsic growth programs on regrowth of corticospinal tract (CST) axons after contusive injury. In the first study, we use self-complimentary adeno associated viral (scAAV) vectors to trace long descending tracts in the spinal cord. We demonstrate clear and bright labeling of cortico-, rubro- and reticulospinal pathways without the need for IH, and show that scAAV vectors transduce more efficiently than single stranded AAV (ssAAV) in neurons of both injured and uninjured animals. This study demonstrates the usefulness of these tracers in highlighting pathways descending from the brain. Retrograde tracing is also a key facet of neuroanatomical studies involving long distance projection neurons. In the next study, we highlight a lentivirus that permits highly efficient retrograde transport (HiRet) from synaptic terminals within the cervical and lumbar enlargements of the spinal cord. By injecting HiRet, we can clearly identify supraspinal and propriospinal circuits innervating MN pools relating to forelimb and hindlimb function. We observed robust labeling of propriospinal neurons, including high fidelity details of dendritic arbors and axon terminals seldom seen with chemical tracers. In addition, we examine changes in interneuronal circuits occurring after a thoracic contusion, highlighting populations that potentially contribute to spontaneous behavioral recovery in this lesion model. In a related study, we use a modified version of HiRet as part of a multi-vector system that synaptically silences neurons to explore the contribution of the rubrospinal tract (RST) and CST to forelimb motor behavior in an intact rat. This system employs Tetanus toxin at the neuronal synapse to prevent release of neurotransmitter via cleavage of vesicle docking proteins, effectively preventing the propagation of action potentials in those neurons. We find that shutdown of the RST has no effect on gross forelimb motor function in the intact state, and that shutdown of a small population of CST neurons in the FMC has a modest effect on grip strength. These studies demonstrate that the HiRet lentivirus is a unique tool for examining neuronal circuitry and its contribution to function. In the final study, we explore stimulation of the Phosphoinositide 3-kinase/Rac-alpha serine/threonine Protein Kinase (PI3K/AKT) growth pathway by antagonizing phosphatase and tensin homolog (PTEN), a major inhibitor, to encourage growth of CST axons after a contusive injury. We use systemic infusions of four distinct PTEN antagonist peptides (PAPs) targeted at different sites of the PTEN protein. We find robust axonal growth and sprouting caudal to a contusion in a subset of animals infused with PAPs targeted to the PTEN enzymatic pocket, including typical morphology of growing axons. Serotonergic fiber growth was unaffected by peptide infusion and did not correlate with CST fiber density. Though some variability was seen in the amount of growth within our animal groups, we find these PTEN antagonist peptides a promising and clinically relevant tool to encourage CST sprouting, and a potentially useful addition to therapies using combinatory strategies to enhance growth. These studies demonstrate that viral tracing is a powerful tool for mapping spinal pathways and elucidating their ability to reform spinal circuits after injury. Viral vectors can be used in both anterograde and retrograde tracing studies to highlight intricacies of neuronal cell bodies, axons and dendritic arbors with a high degree of fidelity. In the injured state, these tools can help identify pathways that contribute to spontaneous recovery of function by highlighting those that reform circuits past an injury site. In the uninjured state, these vectors can contain neuronal silencing methods that help define the contribution of specific pathways to behavior.
Temple University--Theses
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Scali, Manuela. "Fluoxetine treatment promotes functional recovery in a rat model of cervical spinal cord injury." Doctoral thesis, Scuola Normale Superiore, 2014. http://hdl.handle.net/11384/85978.
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