| Project/Area Number |
14580792
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
神経・脳内生理学
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
YAMAMOTO Satoshi Hyogo College of Medicine, Faculty of Medicine, Associate Professor, 医学部, 助教授 (60220464)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Glial cell / Astrocyte / Brain ischemia / Patch-clamp / Membrane current / Glutamate / Glutamate receptors |
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| Research Abstract |
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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