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Study of glial cell function during brain ischemia

Study of glial cell function during brain ischemia
脑缺血时胶质细胞功能的研究
批准号:
14580792
负责人:
YAMAMOTO Satoshi
金额:
$2.3万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2002
资助国家:
日本
项目状态:
已结题
起止时间:
2002 至 2003

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中文摘要
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英文摘要
Purpose : Study of functional changes in electrical membrane properties and chemical receptivity of astrocytes during in vitro ischemia.Method : Using whole-cell patch-clamp techniques, membrane currents were monitored from single cultured astrocyte, and the effects of in vitro ischemia on the electrical membrane properties and receptivity for neurotransmitter, glutamate were examined. Ischemic condition was made by perfusing cells with glucose-free and metabolic inhibitor-containing solution instead of normal artificial cerebrospinal fluid.Results : Ischemic solution caused a transient inward current followed by a slow outward current in the membrane of astrocytes recorded. From the reversal potential, it was suggested that chloride channels and potassium channels might be involved in the generation of the transient inward currents and the slow outward currents, respectively. Glutamate caused inward currents in the astrocyte. The glutamate-induced currents were inhibited by NMDA and non-NMDA glutamate receptor antagonists by about 50%, indicating that astrocytes have not only ionotropic glutamate receptor but also metabotropic glutamate receptors and/or glutamate transporters. The glutamate-induced currents were not modified by ischemic condition in the early time. Due to difficulties of continuous recording, the late effect of ischemia could not be monitored.Conclusion : The astrocyte that has been seemed to be a ischemia-resistant cell, behaves like as the neuron in the electrical membrane properties against ischemia. This suggests that glial cell function can be altered during ischamia, so that maintenance of extracellular concentrations of potassium and neurotransmitters by glial cells might be disturbed.
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Saitoh.M., Yamamoto, S.他: "Arachidonic acid peroxides induce apoptotic Neuro-2A cell death in association with intracellular Ca^<2+> rise and mitochondrial damage independently of caspase-3 activation."Brain Research. 991. 187-194 (2003)
Saitoh.M.、Yamamoto, S.等人:“花生四烯酸过氧化物诱导细胞凋亡性Neuro-2A细胞死亡,与细胞内Ca 2+ 升高和线粒体损伤相关,与caspase-3激活无关。”Brain Research 991。 187-194(2003)
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通讯作者:
Niiyama, S., Yamamoto, S.et al.: "Bupivacaine, but not tetracaine, protects against the in vitro ischemic insult of rat hippocampal CA1 neurons."Neurosci.Res.. 42. 231-241 (2002)
Niiyama, S., Yamamoto, S.et al.:“布比卡因(而非丁卡因)可保护大鼠海马 CA1 神经元免受体外缺血性损伤。”Neurosci.Res.. 42. 231-241 (2002)
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通讯作者:
Ohta, K., Yamamoto, S.et al.: "Stearic acid facilitates hippocampal neurotransmission by enhancing nicotinic ACh receptor responses via a PKC pathway."Brain Res.Mol.Brain Res.. 119. 83-89 (2003)
Ohta, K., Yamamoto, S.等人:“硬脂酸通过 PKC 途径增强烟碱 ACh 受体反应,从而促进海马神经传递。”Brain Res.Mol.Brain Res.. 119. 83-89 (2003)
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Tozaki, H., Yamamoto, S.他: "The inhibitory and facilitatory actions of amyloid-beta peptides on nicotinic ACh receptors and AMPA receptors"Biochem Biophys Res Commun. 294. 42-45 (2002)
Tozaki,H.,Yamamoto,S.等人:“淀粉样蛋白-β肽对烟碱ACh受体和AMPA受体的抑制和促进作用”Biochem Biophys Res Commun.294.42-45(2002)。
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