Expression of brain-derived neurotrophic factor in reactive astrocytes provides neuroprotection to SH-SY5Y cells against six-hydroxydopamine toxicity invitroTsang, Yuen Ting 01 January 2012 (has links)
No description available.
Ferrazzoli, Alexander E.
Thesis (M.A.) -- Central Connecticut State University, 2007. / Thesis advisor: Cheryl L. Watson. "... in partial fulfillment of the requirements for the degree of Master of Arts in Biomolecular Sciences." Includes bibliographical references (leaves 43-46). Also available via the World Wide Web.
Mechanisms involved in protective effects of ischemia-preconditioned neurons on astrocytes against ischemia-induced injury. / 神經元缺血預適應對星形膠質細胞缺血損傷的保護作用及其機制 / CUHK electronic theses & dissertations collection / Shen jing yuan que xue yu shi ying dui xing xing jiao zhi xi bao que xue sun shang de bao hu zuo yong ji qi ji zhiJanuary 2011 (has links)
Wu, Xiaomei. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 163-194). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong,  System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.
Composition and functional studies of chondroitin sulfate proteoglycans at borders between astrocytes and Schwann cells inrelation to axonal crossingLiu, Hengying., 劉恆穎. January 2005 (has links)
published_or_final_version / abstract / Biochemistry / Doctoral / Doctor of Philosophy
The role of lactate in supporting neuronal survival and synaptic function after oxygen and glucose deprivation in the rat hippocampusCater, Heather Lucy January 1999 (has links)
No description available.
No description available.
Composition and functional studies of chondroitin sulfate proteoglycans at borders between astrocytes and Schwann cells in relation to axonal crossingLiu, Hengying. January 2005 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.
Sauzier, Jean-Marc A, Eidson, Lori N
06 May 2012
Morphine is one of the most commonly prescribed medications for the relief of prolonged pain. Both basic science and clinical studies indicate that females require 2-3 times more morphine than males to achieve the same analgesic effect. To date, the mechanisms underlying sex differences in opiate responsiveness are unknown. Recent studies suggest that glial cells are potent modulators of morphine-based analgesia, and in particular, decrease the analgesic effect of opiates. Therefore, we tested the hypothesis that the sexually dimorphic effects of morphine were due to sex differences in glial cell activity. Our studies focused on the midbrain periaqueductal gray (PAG) as this region of the brain is critical for the analgesic effects of morphine. Adult male and female Sprague Dawley rats (250g- 400g) were procured from Charles River Laboratories, and were allowed 7 days to acclimate to the new facility. On the day of the experiment, animals received a subcutaneous injection of morphine (5mg/kg) or were handled in a similar manner. Thirty or 60 minutes after injections or handling, animals were perfused with a 4% paraformaldehyde and 2.5% acrolein tissue fixative solution. Brains were removed and stored in 20% sucrose until ready for sectioning. Brains were sectioned at 25mm using a freezing microtome, and immunohistochemical localization of markers for astrocyte glial cell activity was performed. Antibodies to glial fibrillary acidic protein (GFAP) were used to label activated astrocytes. If our hypothesis is correct, then females will have significantly greater density of the astrocyte cell activity marker GFAP as compared with males. Sex differences in PAG glial cell activity may provide the biological bases for the sexually dimorphic effect of morphine. This research may lead to better treatment for females experiencing prolonged chronic or neuropathic pain.
The identification of 14-3-3[gamma] in astrocytes and its mechanism in protecting astrocytes from ischemia /Chen, Xiaoqian. January 2002 (has links)
Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002. / Includes bibliographical references (leaves 180-202). Also available in electronic version. Access restricted to campus users.
Chen, Samantha M. Y., 陳雯英.
Endothelin-1 (ET-1), a 21-amino acid peptide, exerts multiple functions including vasoconstriction, neurotransmission and neuromodulation. The correlation between ET-1 and pain was examined by localized injection into the animal showing that pain response was induced in the peripheral nervous system, but reduced in the central nervous system. In addition, the pathogenic effect of ET-1 in the nervous system was found to be cell-type specific as ET-1 expression was significantly induced in the astrocytes under certain pathological conditions such as stroke and Alzheimer’s disease. Therefore, in this study, it aims to determine the role of astrocytic ET-1 in inflammatory pain. To better illustrate such notion, transgenic mouse line over-expressing ET-1 in the astrocytes (GET-1) was generated. Under physiological conditions in GET-1 mice, it was revealed that its gross anatomy, in addition with thermal heat and mechanical pain-thresholds, were indistinguishable between GET-1 and its age-matched non-transgenic control (NTg). Inflammatory pain was then induced in the GET-1 mice and NTg mice by subcutaneous formalin injection. Spontaneous and heat-induced pain response were evaluated and analyzed based on the two phases of pain response (i.e. acute and tonic responses). Our results indicated that GET-1 mice exhibited less inflammatory pain-like response when compared to the NTg control, implicating that astrocytic ET-1 over-expression modulates inflammatory pain response. The molecular mechanism substantiating the reduction in this response may be due to the basal expression of pain-mediators in GET-1 mice. Further results showed that over-expression in astrocytic ET-1 evoke an up-regulation in calcitonin gene-related peptide (CGRP) as well as the glutamate transporter-1 (GLT-1), also known as excitatory amino-acid transporters (EAAT2). In addition, under formalin-induced pathological pain, over-expression in astrocytic ET-1 was found to negatively regulate GLT-1 transcription. These findings elucidate the extent that ET-1 contributes to the inflammatory pain pathway via ET-1 and GLT-1 interactions. Overall, this study not only pointed out the involvement of astrocytic ET-1 in inflammatory pain processing, but it also warrants further investigation into the molecular mechanism and potential therapeutic intervention of ET-1-mediated pain. / published_or_final_version / Anaesthesiology / Master / Master of Philosophy
Page generated in 0.1029 seconds