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1
Hart, Andrew McKay. "Peripheral nerve injury : primary sensory neuronal death & regeneration after chronic nerve injury." Thesis, University of Glasgow, 2001. http://theses.gla.ac.uk/4472/.
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After a defined unilateral sciatic nerve transection in the rat, a novel triple staining technique was employed in order to enable the detection of neuronal death in L4 & L5 dorsal root ganglia by light microscopic morphology, and TdT Uptake Nick-End Labelling (TUNEL). Optical dissection was then used to quantify neuronal loss from statistically unbiased estimates of the number of surviving neurons. Neuronal death was demonstrated to begin within 24 hours of injury and to peak 2 weeks later, while neuronal loss plateaued 2 months after axotomy, and 39.2% of neurons died overall. Thus the most relevant experimental timepoints at which to examine the effects of putative neuroprotective strategies are 2 weeks and 2 months after axotomy, until which time a window of opportunity exists for therapeutic intervention. The principal that sensory outcome might be related to the delay between injury and nerve repair was confined by the fact that although surgical nerve repair reduced neuronal death 2 weeks after axotomy, the neuroprotective benefit depended upon how soon after injury the nerve was repaired. Even immediate repair did not entirely eliminate neuronal loss, confirming the need for an adjuvent therapy. Hence the effect of two promising agents with established clinical safety records was examined. N-acetyl-cysteine (NAC) is a clinically proven glutathione substrate antioxidant, and anti-mitotic properties. Systemic treatment caused a dose-dependent improvement in neuronal morphology, a significant reduction in the number of TUNEL positive neurons 2 weeks after axotomy (p<0.05), and 2 months after axotomy it was found to have reduced neuronal loss from 35% to only 3% (p<0.001). L-acetyl-carnitine (LAC) is a physiological peptide integral to mitochondrial aerobic glycolysis that was found to be even more neuroprotective than NAC, since after LAC treatment no neuronal loss was detected 2 months after axotomy (no treatment 35% loss; high-dose LAC -4% loss, p<0.001).
2
Baillie, Andrew G. S. "Skeletal muscle metabolism after nerve crush injury." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU059079.
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A model was developed in the rat using a nerve crush procedure, as a form of temporary denervation, to block neural input to the hindlimb muscle of one leg. The nerve crush has the advantage of allowing self-reinnervation of the muscles after regrowth of the damaged nerve, which occurred (in this study) after approximately 14 days. The initial denervation-like phase resulted in a large loss of muscle mass over the subsequent few days which was mostly through a loss of muscle protein. The results demonstrate the correlation between the concentration of glutamine in the muscles and the rate of protein synthesis over the first 3 days after the nerve crush, but other metabolites (alanine, lactate, and glutamate) were seen to react much more rapidly, with significant changes recorded in the first hour after injury. Further studies were undertaken in an attempt to find a link between these acute changes and the later changes in protein and glutamine metabolism. It was demonstrated that these rapid changes were not as a result of a local hypoglycemia, although a reduction in the rate of in vivo glucose uptake was reduced within 4 hours of the nerve crush. Similarly, measurement of activities of key glycolytic enzymes suggested that there were no acute changes in flux through the glycolytic pathway. Finally, a difference in regional blood flow was demonstrated in the experimental muscles and it was concluded that the acute changes in metabolite concentrations might result from simple physiological changes, in response to the anaesthesia and/or the surgical procedure, which subsequently resolved in the innervated, but not the nerve-deprived, muscles.
3
Rosenthal, Oren D. "Peripheral nerve repair using biomaterial nerve guides containing guidance channels." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000467.
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Welin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.
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Fitton, Anthony Robert. "Muscle recovery following peripheral nerve injury and repair." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418071.
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Lidman, Olle. "Genetics and inflammation in nerve injury-induced neurodegeneration /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-654-5/.
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Wallin, Johan. "Experimental nerve injury-induced pain : mechanisms and modulation/." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-849-1/.
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Bridges, Daniel Robert. "Cannabinoid receptors and pain following peripheral nerve injury." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407774.
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Qudairat, E. "Thermographic evaluation of nerve injury following facial fracture." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479394.
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Archer, D. R. "Axonal transport and related responses to nerve injury." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234835.
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Renton, Tara Frances. "Lingual nerve injury related to third molar surgery." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408264.
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Carty, L. M. "The role of autophagy in peripheral nerve injury." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1396236/.
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Nerve transection injury leads to Wallerian degeneration, involving axonal breakdown, Schwann cell demyelination and Schwann cell transdifferentiation to the Bungner repair cell. Schwann cells participate in demyelination in two ways: indirectly through recruitment of blood-borne phagocytic macrophages and also by a direct, intrinsic mechanism of myelin fragmention and digestion. The lysosome has been implicated in Schwann cell myelin digestion but vesicle pathways in Schwann cells have not been thoroughly investigated. Autophagy is a lysosome-dependent, vesicular degradation pathway directed towards bulk intracellular proteins and was investigated in this study as a potential mechanism for Schwann cell mediated demyelination. Autophagy was found to be strongly induced in response to nerve injury, concomitant with the onset of Schwann cell mediated demyelination, in vitro and in vivo. Autophagy levels were down regulated once demyelination was complete. The expression pattern of GFP-LC3 confirmed that Schwann cells formed autophagosomes in response to nerve injury. Inhibition of autophagy in Schwann cells using pharmacological inhibitors and Atg7fl=flP0-cre mice led to a severe defect in demyelination in response to injury, in vitro and in vivo. Myelin protein and lipid degradation as a marker for demyelination was strikingly reduced in the absence of Schwann cell autophagy and the emergence of structural demyelination features was also delayed. Myelin vesicles were found to accumulate ULK1 in Atg7 null Schwann cells. Myelin vesicles were also shown to be surrounded by GFP-LC3 autophagosomes and it is therefore proposed that the interaction of ULK1 and myelin leads to the formation of autophagosomes on myelin vesicles, which would result in subsequent delivery of myelin to the lysosome. Demyelination-associated autophagy was shown to be promoted by the Schwann cell JNK/c-Jun pathway. Autophagy was shown to be misregulated in a mouse model of demyelinating peripheral neuropathy. In addition, CNS nerve fibers were found not to induce autophagy during demyelination in vitro. Autophagy is therefore likely to be an important determinant of demyelination in the PNS and may represent a differential response to injury between the PNS and CNS.
13
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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Lee, Sena. "ATP and its receptors in nerve injury and repair." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8668.
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Unlike the peripheral nervous system (PNS), adult neurons in the central nervous system (CNS) have limited regenerative capacity after injury. One interesting phenomenon observed nearly four decades ago was that lesion of a peripheral nerve can significantly enhance the regenerative capacity of the central axons of the corresponding dorsal root ganglion (DRG) neurons, termed a ‘conditioning lesion’, but the underlying mechanism is still not fully understood. Since ATP is released after nerve injury and extracellular ATP has a broad range of biological activities, we postulated that ATP might be the injury signalling molecule that triggers the regenerative machinery in the injured neurons. If that were the case, injection of ATP into a peripheral nerve should be able to mimic the effect of a conditioning lesion. To test this theory, we injected ATP into a peripheral (sciatic) nerve after a dorsal column transection and found that ATP injection did promote the regeneration of injured axons into the lesion cavity. We also found that ATP injection activated transcription factor STAT3 and increased the expression of growth associated protein 43 (GAP43) in the corresponding DRG neurons. ATP injection increased the concentrations of ciliary neurotrophic factor and interleukin-6 in sciatic nerve and DRG. These results indicate that intraneural injection of ATP can mimic conditioning lesion to a certain degree. Most interestingly, we found that a second injection of ATP one week after the first one markedly boosted the effects of the first injection as many more axons grew into or across the lesion compared with double saline injection or ATP plus saline injection. Double ATP injection is also more effective in sustaining the expression of phospho- STAT3 and GAP43. Immunohistochemical analysis showed ATP injection caused little Wallerian degeneration at the injection site. Behavioural tests showed no long-term adverse effects to the injected sciatic nerve. In order to explore the underlying mechanism of ATP induced elevation of the regeneration state of DRG neurons and look for more potent purinoceptor agonists to stimulate axonal regeneration, we first tried to identify the expression of purinoceptor subtypes in sciatic nerves using quantitative PCR and immunohistochemistry. We found that mRNAs for all the four P1 and fourteen P2 purinoceptor subtypes were expressed in the sciatic nerve, DRG or dissociated Schwann cells at various levels. Immunohistochemical analysis showed that purinoceptor subtypes are expressed by different types of cells. Due to the expression of nearly all purinoceptor subtypes in the sciatic nerve, it will be a big challenge to identify the receptor subtype(s) responsible for ATP induced axonal regeneration. We have set up a compartmented co-culture system to test various agonists/antagonists of purinoceptors. Taken together, we have shown that intraneural ATP injection can mimic conditioning lesion in promoting sensory axonal regeneration. Identification of the receptor subtype(s) and other molecules involved in the enhanced regeneration capacity of injured neurons may lead to the development of therapeutic agents to effectively promote the axonal regeneration of both peripheral and central neurons.
15
Ohlsson, Marcus. "On optic nerve injury : experimental studies on axonal regeneration in the adult mammalian CNS /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-656-1.
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Jergović, Davor. "Facial nerve injury and microsurgical repair : experimental and clinical studies /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med716s.pdf.
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Lee, I.-Hui. "On CNS injury and olfactory ensheathing cell engraftment strategies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-551-8/.
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Shembesh, Hisham. "The effect of inflammatory cytokines on functional nerve recovery following peripheral nerve injury and repair." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/21458/.
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Swanberg, Maria. "Genetic regulation of nerve injury-induced neurodegeneration and inflammation /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-328-3/.
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Wiberg, Rebecca. "An exploration of the mechanisms behind peripheral nerve injury." Doctoral thesis, Umeå universitet, Anatomi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-127357.
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Despite surgical innovation, the sensory and motor outcome after peripheral nerve injury is incomplete. In this thesis, the biological pathways potentially responsible for the poor functional recoveries were investigated in both the distal nerve stump/target organ, spinal motoneurons and dorsal root ganglia (DRG). The effect of delayed nerve repair was determined in a rat sciatic nerve transection model. There was a dramatic decline in the number of regenerating motoneurons and myelinated axons found in the distal nerve stumps of animals undergoing nerve repair after a delay of 3 and 6 months. RT-PCR of the distal nerve stumps showed a decline in expression of Schwann cells (SC) markers, with a progressive increase in fibrotic and proteoglycan scar markers, with increased delayed repair time. Furthermore, the yield of SC which could be isolated from the distal nerve segments progressively fell with increased delay in repair time. Consistent with the impaired distal nerve stumps the target medial gastrocnemius (MG) muscles at 3- and 6-months delayed repair were atrophied with significant declines in wet weights (61% and 27% compared with contralateral sides). The role of myogenic transcription factors, muscle specific microRNAs and musclespecific E3 ubiquitin ligases in the muscle atrophy was investigated in both gastrocnemius and soleus muscles following either crush or nerve transection injury. In the crush injury model, the soleus muscle showed significantly increased recovery in wet weight at days 14 and 28 (compared with day 7) which was not the case for the gastrocnemius muscle which continued to atrophy. There was a significantly more pronounced up-regulation of MyoD expression in the denervated soleus muscle compared with the gastrocnemius muscle. Conversely, myogenin was more markedly elevated in the gastrocnemius versus soleus muscles. The muscles also showed significantly contrasting transcriptional regulation of the microRNAs miR-1 and miR-206. MuRF1 and Atrogin-1 showed the highest levels of expression in the denervated gastrocnemius muscle. Morphological and molecular changes in spinal motoneurons were compared after L4-L5 ventral root avulsion (VRA) and distal peripheral nerve axotomy (PNA). Neuronal degeneration was indicated by decreased immunostaining for microtubule-associated protein-2 in dendrites and synaptophysin in presynaptic boutons after both VRA and PNA. Immunostaining for ED1-reactive microglia and GFAPpositive astrocytes was significantly elevated in all experimental groups. qRT-PCR analysis and Western blotting of the ventral horn from L4-L5 spinal cord segments revealed a significant upregulation of apoptotic cell death mediators including caspases-3 and -8 and a range of related death receptors following VRA. In contrast, following PNA, only caspase-8 was moderately upregulated. The mechanisms of primary sensory neuron degeneration were also investigated in the DRG following peripheral nerve axotomy, where several apoptotic pathways including those involving the endoplasmic reticulum were shown to be upregulated. In summary, these results show that the critical time point after which the outcome of regeneration becomes too poor appears to be 3-months. Both proximal and distal injury affect spinal motoneurons morphologically, but VRA induces motoneuron degeneration mediated through both intrinsic and extrinsic apoptotic pathways. Primary sensory neuron degeneration involves several different apoptotic pathways, including the endoplasmic reticulum.
21
Ahmed, Saif. "HCN1 Immunoreactivity of α-motoneurons Following Peripheral Nerve Injury." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1340820984.
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Hawk, Kiel W. "Retrograde influences of peripheral nerve injury on uninjured neurons." Miami University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=miami1387231538.
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McKay, Hart Andrew. "Sensory neuronal protection & improving regeneration after peripheral nerve injury." Doctoral thesis, Umeå universitet, Handkirurgi, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-52.
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Peripheral nerve trauma is a common cause of considerable functional morbidity, and healthcare expenditure. Particularly in the ~15% of injuries unsuitable for primary repair, standard clinical management results in inadequate sensory restitution in the majority of cases, despite the rigorous application of complex microsurgical techniques. This can largely be explained by the failure of surgical management to adequately address the neurobiological hurdles to optimal regeneration. Most significant of these is the extensive sensory neuronal death that follows injury, and which is accompanied by a reduction in the regenerative potential of axotomised neurons, and in the supportive capacity of the Schwann cell population if nerve repair is delayed. The present study aimed to accurately delineate the timecourse of neuronal death, in order to identify a therapeutic window during which clinically applicable neuroprotective strategies might be adopted. It then proceeded to investigate means to increase the regenerative capacity of chronically axotomised neurons, and to augment the Schwann cells’ ability to promote that regenerative effort. Unilateral sciatic nerve transection in the rat was the model used, initially assessing neuronal death within the L4&5 dorsal root ganglia by a combination of morphology, TdT uptake nick-end labelling (TUNEL), and statistically unbiased estimation of neuronal loss using the stereological optical disector technique. Having identified 2 weeks, and 2 months post-axotomy as the most biologically relevant timepoints to study, the effect upon neuronal death of systemic treatment with acetyl-L-carnitine (ALCAR 10, or 50mg/kg/day) or N-acetyl-cysteine (NAC 30, or 150mg/kg/day) was determined. A model of secondary nerve repair was then adopted; either 2 or 4 months after unilateral sciatic nerve division, 1cm gap repairs were performed using either reversed isografts, or poly-3-hydroxybutyrate (PHB) conduits containing an alginate-fibronectin hydrogel. Six weeks later nerve regeneration and the Schwann cell population were quantified by digital image analysis of frozen section immunohistochemistry. Sensory neuronal death begins within 24 hours of injury, but takes 1 week to translate into significant neuronal loss. The rate of neuronal death peaks 2 weeks after injury, and neuronal loss is essentially complete by 2 months post-axotomy. Nerve repair is incompletely neuroprotective, but the earlier it is performed the greater the benefit. Two clinically safe pharmaceutical agents, ALCAR & NAC, were found to virtually eliminate sensory neuronal death after peripheral nerve transection. ALCAR also enhanced nerve regeneration independently of its neuroprotective role. Plain PHB conduits were found to be technically simple to use, and supported some regeneration, but were not adequate in themselves. Leukaemia inhibitory factor enhanced nerve regeneration, though cultured autologous Schwann cells (SC’s) were somewhat more effective. Both were relatively more efficacious after a 4 month delay in nerve repair. The most profuse regeneration was found with recombinant glial growth factor (rhGGF-2) in repairs performed 2 months after axotomy, with results that were arguably better than were obtained with nerve grafts. A similar conclusion can be drawn from the result found using both rhGGF-2 and SC’s in PHB conduits 4 months after axotomy. In summary, these findings reinforce the significance of sensory neuronal death in peripheral nerve trauma, and the possibility of its` limitation by early nerve repair. Two agents for the adjuvant therapy of such injuries were identified, that can virtually eliminate neuronal death, and enhance regeneration. Elements in the creation of a bioartificial nerve conduit to replace, or surpass autologous nerve graft for secondary nerve repair are presented.
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Whiteside, Garth Thomas. "Cell death in the nervous system after peripheral nerve injury." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624387.
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Erichsen, Helle Kirstein. "Characterisation of the spared nerve injury model of neuropathic pain /." Cph. : The Danish University of Pharmaceutical Scienes, Department of Pharmacology, NeuroSearch, Kongl. Carolinska Medico Chirurgiska Institutet, 2003. http://www.dfh.dk/phd/defences/Hellekirsteinerichsen.htm.
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Lam, Wai-yuan Leon. "Neuroprotection of low energy laser on retinal ganglion cells survival after optic nerve injury /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2207904X.
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Zeng, Qingrong, and 曾慶榮. "The effect of intravitreal administration of peripheral nerve grafts or trophic factors on axonal regeneration of retinal ganglion cellsfollowing a crush injury of the optic nerve." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31220265.
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冼振鋒 and Chun-fung Sin. "Olfactory ensheathing cell transplanation in spinal cord after contusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738930.
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Sin, Chun-fung. "Olfactory ensheathing cell transplanation in spinal cord after contusion injury." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738930.
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Bongenhielm, Ulf. "Structure and function of trigeminal primary sensory neurons after peripheral nerve injury /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3954-3/.
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Hay, Catriona Helen. "Injury responses in the spinal cord : gene expression studies." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244087.
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Vora, Amit Rajni. "Light and electron microscopical studies on the structure of traumatic neuromas of the human lingual nerve." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269373.
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Myles, Lynn M. "Anatomical and physiological studies of the recovery of peripheral nerve function following repair with freeze-thawed skeletal muscle autografts." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/20052.
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Roosevelt, Rodney W. "INVESTIGATIONS INTO THE EFFECTS OF ELECTRICAL STIMULATION OF THE VAGUS NERVE ON NOREPINEPHRINE IN THE CORTEX AND HIPPOCAMPUS OF EXPERIMENTALLY BRAIN INJURED AND UNINJURED RATS." OpenSIUC, 2013. https://opensiuc.lib.siu.edu/dissertations/699.
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The vagus nerve is the principal pathway by which autonomic sensory information is carried from the periphery to the CNS where it influences the activity of a numerous structures including the locus coeruleus. Electrical stimulation of the vagus nerve has been demonstrated to enhance performance in a variety of memory tasks in both rats and humans and is used clinically for the control of epilepsy in humans. Electrical stimulation of the vagus nerve has also been shown to improve functional recovery following experimental brain injury in rats. The central hypothesis in these experiments is that vagus nerve stimulation exerts its beneficial effects by mediating the release of norepinephrine in the CNS. The results from Experiment I indicate that VNS results in increased extracellular NE concentration in the hippocampus at both the 0.5 and 1.0 mA stimulus intensities, and in the cortex at the 1.0 mA intensity. Increased concentrations of extracellular NE induced by VNS, regardless of structure, were transient, dissipating before the subsequent baseline recording period. Further, VNS-induced alterations in extracellular NE concentrations were observed bilaterally. Insult to the CNS by means of FPI resulted in long lasting depression of extracellular NE concentrations in the cortex of the injured controls and 1.0 mA VNS group that was partially attenuated 1.0 mA VNS. In the 0.5 mA VNS group NE concentrations remained above pre-injury levels for the majority of the post-FPI measurement period. In the hippocampus, mean NE concentrations in the period immediately following FPI were decreased in comparison to pre-FPI concentrations. Concentrations of hippocampal NE remained depressed in the injured control group throughout the 48 hr sample period. Hippocampal NE concentrations in both the 0.5 mA VNS and 1.0 mA VNS group recovered to above pre-injury levels by 14-20 hrs post-FPI and were significantly higher than that of the injured controls in the 20-26 and 26-32 hr post-FPI sampling periods. Further, hippocampal NE concentrations remained significantly higher in 0.5 mA VNS group in comparison to injured controls in the 32-38 and 38-44 hr sampling periods.
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Mullins, Fraser Hewitt. "Post-translational processing of microtubule protein during peripheral nerve regeneration." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385223.
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Zeng, Qingrong. "The effect of intravitreal administration of peripheral nerve grafts or trophic factors on axonal regeneration of retinal ganglion cells following a crush injury of the optic nerve /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19882051.
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Yang, In Hong. "The study of the neurophysiology of high strain rate nerve injury." Texas A&M University, 2003. http://hdl.handle.net/1969.1/416.
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The study of the mechanism of traumatic brain injury (TBI) processes at the cellular level is vital to obtain characterization of nerve cell damage after mechanical deformation. This understanding is needed to find feasible therapeutic targets for mechanically damaged neurons. To study the cellular level of TBI damage, development of a new in vitro cellular model of TBI might be done to simulate in vivo cellular TBI.
In this research, two studies were performed: (1) the design and construction of an in vitro cell stretching device to mechanically injure cells and (2) the characterization of the molecular and cellular level of the TBI mechanism. The cell stretching device design allows for the precise control of cell strain and duration of stretching cells such that TBI can be mimicked. Analysis of the cellular and molecular level mechanisms of TBI in the proposed in vitro model might help in the design of therapeutic strategies for the treatment of TBI. Our proposed mechanism of injury due to TBI is as follows: after the cell is stretched, a cellular signaling molecule is released to activate the cellular signaling pathway. The activated cell signal may activate kinases which phosphorylate proteins and initiate new protein synthesis. Newly phosphorylated and synthesized proteins may activate the apoptotic process.
Using a variety of pharmacological agents, one could block steps in the hypothesized mechanism and examine the effect of those agents on downstream cellular processes and cell apoptosis. For example, the inhibitions of calcium transport, protein synthesis, and caspases were performed to examine the initial activation of the signaling pathway and the role of both in the apoptosis process. Proteomics of TBI may help the understanding of the mechanism of TBI related protein expression. This work will contribute to the discovery of new therapeutic targets and better treatments for TBI.
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Kiesewetter, Hannes. "Epidermal growth factor receptor ligands as modulators of peripheral nerve injury." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/epidermal-growth-factor-receptor-ligands-as-modulators-of-peripheral-nerve-injury(d475ff9b-b2b2-40cd-a979-bac74f757475).html.
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Signalling between different cell types in the nervous system is a key element in the pathophysiology of peripheral nerve injury. Epidermal growth factor receptor ligands (EGFRLs) bind the EGF receptor (ErbB1) and its related protein ErbB4 forming an adaptable signalling system implicated in multiple biological processes. Ligands binding the EGF receptor have not yet been implicated in the pathophysiology of nerve injury. In this thesis, I demonstrated differential expression of EGFR ligands following nerve injury in rats, such as Amphiregulin, Epidermal growth factor, Epiregulin, Heparin-binding EGF, Transforming growth factor-α and Betacellulin (BTC). In a medium-throughput quantitative PCR array screening of cytokines, BTC was one of the top differentially upregulated factors following partial sciatic nerve transection (SNT) at different timepoints. Given that its role in the nervous system is unknown I set out to elucidate its mechanism of action following injury. First I examined its ability to activate intracellular pathways. Although BTC activated ERK and p38 MAP kinases in relevant cell types (dorsal root ganglion neurons, macrophages) imaging experiments indicated no change in intracellular calcium levels. To investigate a potential neuronal effect I examined the growth promoting effect of BTC on dissociated DRG neurons. The growth factor did not affect neurite outgrowth. Interestingly, other EGFR ligands were also ineffective. In cultured peritoneal macrophages chemotaxis was not affected in vitro, but I demonstrated a chemotactic effect in vivo. Additionally, examination of a panel of macrophage phenotypic markers revealed a downregulation of the phagocytic scavenger receptor CD36 following stimulation with BTC. Intrathecal injection of BTC in the spinal cord (L4-L5), was able to activate ERK but did not affect thermal (Hargreaves) and mechanical (von Frey) sensitivity. Moreover, blocking the EGF receptor in models of either inflammatory (formalin injection in the hindpaw) or neuropathic (SNT) pain did not alter thermal and mechanical hypersensitivity. In summary, BTC is robustly upregulated following peripheral nerve injury. Although its role its not yet completely clarified, my data points towards a modulating effect on the macrophage phenotype and its an interesting target for future investigation on the pathophysiology of nerve injury.
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Lenihan, David V. "New methods for the repair and assessment of peripheral nerve injury." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/22406.
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The present study was designed to investigate factors which could influence the regeneration of peripheral nerves which had been cut and repaired using a variety of grafting techniques. These methods were: repair with a microwaved muscle autograft, a freeze-thawed muscle autograft, and several groups where repair involved a controlled release biodegradable glass tube containing a variety of factors which have been shown to influence nerve regeneration. Assessment of all of these experimental groups involved the use of established electrophysiological and morphometric techniques but also the development of new techniques for measuring the conduction velocity of the lowest fibres and the variability of reinnervation at the neuromuscular junction (stimulated jitter). The experiments revealed that the microwave muscle graft provided the structural support needed for regeneration, however difficulties in preparing the graft made its use in the clinical setting doubtful. The controlled release glass tube did not interfere with regeneration an supported similar levels of regeneration when compared with an established surgical technique. Jitter proved to be an excellent and highly discriminatory test for assessment of the progression and quality of reinnervation of skeletal muscle. The potential for using these techniques in the experimental and clinical settings is discussed.
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Rode, Frederik. "Pharmacological testing in the spared nerve injury model of neuropathic pain /." Cph. : The Danish University of Pharmaceutical Sciences, Department of Pharmacology, 2005. http://www.dfuni.dk/index.php/Frederik_Rode/1938/0/.
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Kimpton, Amanda-Jane. "Comparative structural analysis of reinnervated muscle following nerve injury and repair." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23076.
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The repair of peripheral nerve injuries is a major reconstructive problem, particularly when direct suturing of a transected nerve is not feasible option. This arises because mechanisms of nerve repair are not fully understood. The purpose of the first group of experiments was to compare methods of nerve repair, including use of novel, biodegradable glass tubes. The possible use of these tubes as a means of confining humoral or cellular substances at the site of repair was also assessed. In a further study, experiments were designed to establish first, the optimal timing of nerve repair (immediate or delayed); second, whether there was a difference in the level of recovery between neonates and adults after nerve repair; third, to assess the freeze-thawed muscle graft (FTMG) method as a surgical technique and to determine whether the FTMG is at least as good as a conventional nerve graft. This investigation was carried out in an animal model of obstetrical brachial plexus palsy (OBPP). Assessment of experimental outcome in both studies was by measurement of the structural and cytochemical changes which occurred in the target muscle after peripheral nerve injury and repair. Morphometric, histochemical and immunocytochemical measurements showed alterations in muscle fibre size and architecture, as well as connective tissue content and the proportions and the distributions of the different fibre types. These changes indicated that after repair with controlled-release glass tubes there was reinnervation of the target muscle, although the results were superior after repair by FTMG. As to whether the potential of nerve to regenerate after repair decreases with age, or whether immediate or delayed repair is best in the treatment of OBPP, the experiments have contributed to solving but have not resolved the dilemma associated with these issues.
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Pettersson, Jonas. "Biosynthetic conduits and cell transplantation for neural repair." Doctoral thesis, Umeå universitet, Institutionen för integrativ medicinsk biologi (IMB), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42440.
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Spinal cord injury results in complete failure of the central neurons to regenerate and is associated with cyst formation and enlargement of the trauma zone. In contrast to the spinal cord, axons in the injured peripheral nerve have the capacity to undergo some spontaneous regeneration. However, significant post-traumatic loss of nervous tissue causing long nerve gap is one of the main reasons for the poor restoration of function following microsurgical repair of injured nerves. The present thesis investigates the effects of biodegradable conduits prepared from fibrin glue and poly-beta-hydroxybutyrate (PHB) in combination with cultured Schwann cells, mesenchymal stem cells and extracellular matrix molecules on regeneration after spinal cord and peripheral nerve injury in adult rats. At 4-8 weeks after transplantation into the injured spinal cord, the PHB conduit was well integrated into the cavity but regenerating axons were found mainly outside the PHB. When suspension of BrdU-labeled Schwann cells was added to the PHB, regenerating axons filled the conduit and became associated with the implanted cells. Modification of the PHB surface with extracellular matrix molecules significantly increased Schwann cell attachment and proliferation but did not alter axonal regeneration. To improve the labeling technique of the transplanted cells, the efficacy of fluorescent cell tracers Fast Blue, PKH26, Vibrant DiO and Cell Tracker™ Green CMFDA was evaluated. All tested dyes produced very efficient initial labeling of olfactory ensheathing glial cells in culture. The number of Fast Blue-labeled cells remained largely unchanged during the first 4 weeks whereas the number of cells labeled with other tracers was significantly reduced after 2 weeks. After transplantation into the spinal cord, Fast Blue-labeled glial cells survived for 8 weeks but demonstrated very limited migration from the injection sites. Additional immunostaining with glial and neuronal markers demonstrated transfer of the dye from the transplanted cells to the host tissue. In a sciatic nerve injury model, the extent of axonal regeneration through a 10mm gap bridged with tubular PHB conduit was compared with a fibrin glue conduit. At 2 weeks after injury, the fibrin conduit supported similar axonal regeneration and migration of the host Schwann cells compared with the PHB conduit augmented with a diluted fibrin matrix and GFP-labeled Schwann cells or mesenchymal stem cells. The long-term regenerative response was evaluated using retrograde neuronal labeling. The fibrin glue conduit promoted regeneration of 60% of sensory neurons and 52% of motoneurons when compared with the autologous nerve graft. The total number of myelinated axons in the distal nerve stump in the fibrin conduit group reached 86% of the nerve graft control and the weight of gastrocnemius and soleus muscles recovered to 82% and 89%, respectively. When a fibrin conduit was used to bridge a 20mm sciatic nerve gap, the weight of gastrocnemius muscle reached only 43% of the nerve graft control. The morphology of the muscle showed more chaotic appearance and the mean area and diameter of fast type fibers were significantly worse than those of the corresponding 10mm gap group. In contrast, both gap sizes treated with nerve graft showed similar fiber size. In summary, these results show that a PHB conduit promotes attachment, proliferation and survival of adult Schwann cells and supports marked axonal growth after transplantation into the injured spinal cord. The data suggest an advantage of the fibrin conduit for the important initial phase of peripheral nerve regeneration and demonstrate potential of the conduit to promote long-term neuronal regeneration and muscle recovery.
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Yen, Laurene Dao-Pei. "Sympathetic sprouting and changes in nociceptive sensory innervation in the glabrous skin of the rat hind paw following partial peripheral nerve injury." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101873.
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Previous studies have suggested that sympathetic sprouting in the periphery may contribute to the development and persistence of sympathetically-maintained pain in animal models of neuropathic pain. The purpose of this thesis was to examine morphological changes in the cutaneous innervation in rats after chronic constriction injury (CCI) to the sciatic nerve. More specifically, this study addresses the question of whether sympathetic fibres sprout de novo into the upper dermis of the rat hindpaw skin after CCI of the sciatic nerve. We also determined changes in peptidergic sensory innervation following CCI.At several periods post-injury, hind paw skin was harvested and processed using a monoclonal antibody against dopamine-beta-hydroxylase to detect sympathetic fibres and a polyclonal antibody against calcitonin gene-related peptide to identify peptidergic sensory fibres. We observed migration and branching of sympathetic fibres into the upper dermis of the hind paw skin, from where they were normally absent. This migration was first detected at 2 weeks, peaked at 4 to 6 weeks and lasted for at least 20 weeks post-lesion. At 8 weeks post-lesion, there was a dramatic increase in the density of peptidergic fibres in the upper dermis. Quantification revealed that densities of peptidergic fibres 8 weeks post-lesion were significantly above levels of sham animals. Interestingly, the ectopic sympathetic fibres did not innervate blood vessels but formed a novel association and wrapped around sprouted peptidergic nociceptive fibres. Our data show a long-term sympathetic and sensory innervation change in the rat hind paw skin after the chronic constriction injury. This novel fibre arrangement after nerve lesion may play an important role in the development and persistence of sympathetically-maintained neuropathic pain after partial nerve lesions.
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Leiva, Rodríguez Tatiana. "Investigation of the role and modulation of autophagy for neuroprotection and nerve regeneration using models of peripheral nerve injury." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/667461.
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Lesiones en el nervio periférico causan una disrupción axonal que puede producir una neurodegeneración retrograda. Las neuronas axotomizadas sufren una serie de cambios fenotípicos a nivel molecular y celular, algunos de ellos llamados mecanismos endógenos de neuroprotección, que promueven la supervivencia neuronal. En estos mecanismos se incluyen la respuesta de proteína desplegada (UPR) y la autofagia.
La intensidad y el tiempo de respuesta de la neurona vienen influenciados por la severidad de la lesión, la distancia respecto al soma, el tipo de neurona y la edad. Sin embargo, cuando la lesión es muy proximal al soma, como es el caso de la lesión de avulsión de raíz de nervio periférico (RA), los mecanismos endógenos de neuroprotección pueden no ser activados contribuyendo a la neurodegeneración. Por este motivo creemos que la corrección o la potenciación de los mecanismos endógenos podrían ser efectivos para la neuroprotección y la regeneración.
Primero caracterizamos el estado de flujo autofágico después de PNI in vivo y encontramos un bloqueo de estas vías, alteraciones en proteínas relacionadas con microtúbulos y proteínas de tráfico vesicular a los 5-7 días posteriores a la lesión. Posteriormente, modelamos algunos eventos concomitantes asociados con las alteraciones de la autofagia y en el citoesqueleto en el modelo in vitro. Además, analizamos la respuesta temporal de la autofagia y el citoesqueleto in vitro. Estos resultados, revelaron que la neurodegeneración podría ocurrir debido a la alteración inicial de los microtúbulos después del bloqueo de la autofagia. Además,estas alteraciones del citoesqueleto aumentan la astrogliosis y la muerte de MN in vivo. Finalmente, exploramos el papel de la potenciación de la autofagia. El análisis del curso temporal de la inducción de autofagia farmacológica usando rapamicina reveló ser neuroprotector solo como un pretratamiento antes de la lesión de RA. Además, la activación de la autofagia mediada por la sobreexpresión de ATG5 dio como resultado una preservación de MN acompañada de una mejora en la vía secretora y el flujo autofagico.
Resultados previos demostraron que BiP neuroprotegía frente a RA y que su expresión se veía disminuida en las motoneuronas degeneradas. Considerando su relación con la autofagia, nuestro objetivo fue aclarar los mecanismos de neuroprotección mediante la proteómica. Descubrimos que la sobrexpresión de GRP78/BiP promovía la reducción de proteínas mitocondriales mediante la inducción de la mitofagia. Esta activación era dependiente de IP3R y PINK1
Finalmente, considerando que una terapia efectiva después de la lesión de nervio periférico promueve el crecimiento axonal y la regeneración nerviosa, exploramos si la potenciación de la autofagia podría ser pro-regenerativa.
Finalmente, considerando que una terapia efectiva después de la PNI debería promover el rebrote axonal y la regeneración nerviosa, exploramos si la estimulación autofagia también podría ser pro-regenerativa. Descubrimos que la autofagia mediada por SIRT-1/ HIF1α promueve el crecimiento de neuritas in vitro. Además, la potenciación de la autofagia mediante la sobrexpresión de ATG5 o SIRT1 acelera la recuperación funcional y el crecimiento axonal después de la lesión.
Estos hallazgos sugieren que la corrección o la potenciación de los mecanismos endógenos como la autofagia, pueden ser una terapia eficaz para aumentar la supervivencia de las motoneuronas desconectadas y mejorar el crecimiento axonal después de las lesiones de nervio periférico.Severe peripheral nerve injury (PNI) cause axonal disruption and may produce retrograde neurodegeneration. Axotomized neurons undergo a series of phenotypic changes at the molecular and cellular levels, some of them called endogenous mechanisms of neuroprotection, that promote neuronal survival that includes the unfolded protein response (UPR), the heat-shock response, the autophagy pathway, the ubiquitin-proteasome system, chaperone, the endoplasmic reticulum (ER)-associated degradation machinery (ERAD) and the antioxidant defence. The intensity and time course of the neuronal response are mainly influenced by the severity of the injury, distance of the lesion to cell body, type of neuron and age. However, when the injury is proximal to the soma, such in the case of peripheral nerve root avulsion (RA), the endogenous mechanisms of neuroprotection might not be properly activated contributing to neurodegeneration. We reasoned that the correction or potentiation of these mechanisms might be effective for neuroprotection. We first characterize the state of autophagy flux after PNI in vivo and found a blockage of these pathway, alterations in microtubule related proteins and vesicle trafficking proteins at 5-7 days post-injury Subsequently, we modelize some concomitant events associated with autophagy failure such as cytoskeleton abnormalities in in vitro model. Furthermore, we analyse the time course response of autophagy and cytoskeleton in vitro. These revealed that neurodegeneration might occur due to initial microtubule alteration followed autophagy blockage. These cytoskeleton alterations increase astrogliosis and MN death in vivo. Finally, we explored the role of autophagy potentiation. Time-course analysis of pharmacological autophagy induction using rapamycin revealed to be neuroprotective only as a pre-treatment before RA injury. In addition, autophagy activation mediated by ATG5 overexpression resulted in a MN preservation accompanied by improved internal trafficking and autophagy flux. Previous data demonstrated neuroprotective capacities mediated by GRP78/BiP overexpression that it has been found downregulated in degenerated MNs after the lesion. Considering its relationship with autophagy, we aimed to clarify the mechanisms of these neuroprotection by proteomic analysis. We discovered that GRP78/BiP overexpression induces the downregulation of mitochondrial proteins by the induction of mitophagy. In this activation of mitophagy by GRP78/BiP is implicated IP3R and PINK1 Finally, considering that an effective therapy after PNI should promote axonal regrowth and nerve regeneration, we explored if autophagy stimulation might be pro-regenerative as well. We did so by overexpressing ATG5 or by genetic and pharmacological activation of SIRT1. We discovered that autophagy mediated by SIRT-1/HIF1α promotes neurite outgrowth in vitro. In addition, autophagy potentiation by ATG5 or SIRT1 overexpression enhances functional recovery and axonal growth after the lesion. Overall, these findings suggested that correction or potentiation of endogenous mechanisms such as autophagy may be an effective therapy to increase the survival of disconnected MNs and enhanced axonal regrowth after the peripheral nerve injuries.
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Schaeffer, Julia. "The molecular regulation of spinal nerve outgrowth." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271632.
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During amniote embryogenesis, the segmented pattern characteristic of the vertebral column appears early during development through the sequential formation of multipotent structures called somites. Somites differentiate subsequently into dermomyotome (giving rise later to skin and skeletal muscles) and sclerotome (giving rise to vertebral bone structures and cartilage). In addition, sclerotomes subdivide following their rostro-caudal intrasegmental boundary into an axon growth-permissive region (anterior half) and an axon growth-repulsive region (posterior half). This binary system instructs motor and sensory axon navigation, as well as neural crest cell migration, to ensure that the peripheral nervous system develops without obstruction by the future cartilage and bones of the vertebral column. Repellent cues are expressed in posterior half-sclerotomes in order to exclude navigating axons from “no-go” areas and restrict their growth to specific exit points of the future vertebral column. Interestingly, similar repellent cues (e.g. Eph/Ephrins) are expressed in the adult central nervous system (CNS) and have been shown to control connectivity and plasticity throughout life. Following brain or spinal cord injury, these repellent molecules are upregulated by reactive astrocytes accumulating at the lesion site, and may impede axon regeneration in this region. In this dissertation, I am presenting the results of a differential gene expression analysis of anterior and posterior half-sclerotomes, based on RNA-sequencing data and using the chick embryo as a model organism. This study led to the identification of molecules, previously uncharacterized in this system, that may play a role in adhesive and mechanical properties of somites and in axon guidance and fasciculation. I focused on the functional analysis of one molecule of the posterior half-sclerotome, the extracellular matrix protein Fibulin-2. To look at its role in the segmentation of spinal axons, I used ectopic misexpression in a subset of segments based on somite electroporation. The width of spinal nerve bundle growth was restricted by Fibulin-2 overexpression in posterior and anterior half-sclerotomes, suggesting a role in sharpening/controlling the path of spinal axon growth. In addition, I showed that this could occur via an interaction with the axon growth repellent Semaphorin 3A. Then I looked at the expression of Fibulin-2 in two models of CNS injury: mouse cerebral cortical stab injury and rat dorsal crush spinal cord injury. In both cases, I observed an increase in Fibulin-2 protein level compared to control. I also used primary cultures of rat cortical astrocytes to show that the expression of Fibulin-2 after inflammatory cytokine-induced activation is increased. Finally, I studied a candidate axon growth repellent previously identified in the laboratory. I explored the hypothesis that this repellent molecule is an O-glycosylated, spliced variant form of a known protein. To characterize this repellent molecule, I used RNA-sequencing data from chick embryonic somites and 2D gel electrophoresis of an astrocytic cell line protein extract. Together, these results suggested that the developing vertebral column and the adult CNS share molecular features to control axon growth and plasticity. This type of study could lead to the characterization of molecular systems that regulate axon growth, and to the identification of novel therapeutic targets in brain or spinal cord injury.
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Roberts, Sheridan. "The control of Schwann cell myelination during development and after nerve injury." Thesis, University of Plymouth, 2016. http://hdl.handle.net/10026.1/5489.
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Schwann cells are the principal glial cell of the peripheral nervous system and are responsible for axon maintenance, regeneration and increasing saltatory conduction of neurons. Schwann cell differentiation and myelination is mediated by a core network of transcription factors and signalling pathways, which have been divided into two groups; positive and negative regulators. Sox10, NFATc4, Oct6, Krox20 and the ERK 1/2 signalling pathway have been characterised as positive regulators of Schwann cell differentiation and myelination; with Sox10 and Krox20 also playing critical roles in myelin maintenance. On the other hand, transcription factors cJun, Pax3, Id2 and signalling pathways Notch and p38 mitogen activated protein (MAP) kinases (MAPK) have been identified as negative regulators of Schwann cell differentiation and myelin formation. Recently, the HMG transcription factor Sox2 was identified as a negative regulator of Schwann cell myelination in vitro, however its role in Schwann cell myelination in vivo has not yet been studied. This study therefore aimed to examine the role of Sox2 overexpression in Schwann cells and how it effects Schwann cell differentiation and myelination during development and after injury. In addition, we aimed to investigate for the first time the specific role of p38α (the major isoform of p38 MAPK) in Schwann cell myelination in vivo, by generating Schwann cell specific p38α conditional knockout mice. Sox2 is highly expressed in immature Schwann cells, but is downregulated as Schwann cells being to mature and differentiate. This study shows that continued expression of Sox2 during development and after injury, impairs Schwann cell differentiation and myelination by directly downregulating the expression of two core transcription factors; Sox10 and Krox20, as well as myelin proteins, P0 and MBP. In addition, we observe that continued Sox2 expression significantly increases Schwann cell proliferation and maintains Schwann cells in an immature state. Unexpectedly, we also observed that continued Sox2 expression significantly increases the number of macrophages present in the nerves of Sox2 overexpressing mice at both P60 and 21 days post injury. Phenotypically, Sox2 overexpressing mice 6 show signs of a peripheral neuropathy and animals have impaired motor and sensory function. These findings confirm that Sox2 is a negative regulator of Schwann cell myelination and suggests that continued Sox2 expression is sufficient to drive the progressive development of a peripheral nerve disorder which may resemble Charcot-Marie-Tooth type 1 demyelinating neuropathy and congenital hypomyelinating neuropathy. As a negative regulator of Schwann cell myelination, activity of the p38 MAPK pathway has been shown to inhibit myelin formation in vitro and to also induce the Schwann cell injury response; by driving Schwann cell dedifferentiation and demyelination following injury. Here we show that specific removal of the p38α isoform in Schwann cells leads to an increase in myelin thickness at early developmental time-points, along with an elevated expression of myelin proteins, P0 and MBP. Further analysis following nerve injury revealed that removal of p38α results in an initial decrease in Schwann cell demyelination, yet improves axon remyelination at 21 days post injury. These results demonstrate the specific role of p38α in regulating Schwann cell myelination, and how it could be a direct therapeutic target for improving nerve repair after injury.
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林瑋源 and Wai-yuan Leon Lam. "Neuroprotection of low energy laser on retinal ganglion cells survivalafter optic nerve injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31222869.
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Mallek, Jennifer de Toledo. "Hyaluronic acid-olfactory ensheathing cell compositions for spinal cord injury nerve regeneration." [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0015880.
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Liu, Liang Qin. "Sacral Nerve Stimulation : The Effect on Gluteal Tissues in Spinal Cord Injury." Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504568.
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Following a spinal cord injury (SCI), up to 85% of individuals develop pressure ulcers (PUs) at some point during their lifetime. Tissue ischemia caused by prolonged localized pressures combined with loss of sensation below the level of injury have been considered the major factors for PUs in SCI. Ischial tuberosities are one of the most common sites of PUs in SCI individuals who use wheelchairs. PUs represent a very significant cost burden for the health and social care system and are extremly difficult to fully repair. Hence, prevention of PUs has been the priority. Specialised cushions to reduce seating pressures combined with pressure relief by the patient perfonning 'push-ups' or 'leaning forward' are presently considered the best options for preventing ischial PUs in SCI population. However, perfonning pressure relief requires good upper limb strength together with continued motivation; which may not always be present in high-level lesion individuals. Furthennore, seat cushions alone do not pennit adequate pressure relief for continuous sitting. The idea of activating paralyzed gluteal muscles through_tl1~~s~ of functional electrical stimulation (FES),has been explored over the past two decades for use in SCI. However, surface FES stimulates the muscles by repeatedly applying large electrodes to the buttocks. The long-tenn practicality and patient compliance with this technique is a problem. It was reported that non-invasive Functional Magnetic Stimulation (FMS) of the sacral nerve roots can activate gluteal muscles. In this thesis, Sacral Anterior Root Stimulator (SARS) implant (currently used for bladderlbowel empty in SCI) is proposed for ischial pressure ulcer prevention in SCI population. The aims of this study are 1)' To investigate the dynamic effects of sacral FMS on seating interface pressure changes in able bodied subjects; and evaluate the efficacy of sacral FMS; 2) To investigate the dynamic effects of sacral FMS on seating interface pressure and cutaneous hemoglobin and oxygenation changes in SCI; and demonstrate its utility as an assessment tool; 3) To show that similar effects are possible with sacral electrical stimulation through a SARS implant device currently used for bladder emptying in SCI. 5 able-bodied volunteers, 11 patients with SCI (6 complete injuries, 5 incomplete injuries) participated in the FMS study. 6 other SCI individuals with a SARS implant were recruited for the SARS study. In order to compare sacral nerve root stimulation against conventional surface FES, 6 complete SCI were included for a surface FES study The results jndicated that sacral nerve root stimulation, either by using FMS or implanted SARS can induce gluteus maximus contractions sufficient to achieve significant changes in ischial pressures and cutaneous hemoglobin and oxygenation during sitting. The magnitude of pressure reduction archived with FMS and SARS were greater than that with conventional surface FES. In addition to these beneficial acute effects, chronic stimulation via a SARS implant may be useful for building gluteal muscle bulk as a further important preventative measure to reduce pressure ulcer in SCI population.
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Jerosch-Herold, Christina. "The clinical assessment of hand sensibility after peripheral nerve injury and repair." Thesis, University of East Anglia, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246673.
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