1996 Fiscal Year Final Research Report Summary
Roles of ATP-sensitive ion channels in neurons
| Project/Area Number |
07670051
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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 |
General physiology
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| Research Institution | Kanazawa University |
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Principal Investigator |
OHNO-SYOSAKU Takako Kanazawa University, Fac, of Med., assistant professor, 医学部, 助教授 (60179025)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Neuron / Hippocampus / Synaptic transmission / Brain ischemia / Presynaptic inhibition / ATP-sensitive K channels / Retrograde messenger |
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| Research Abstract |
Mechanisms of changes in neural activities induced by brain ischemia and the possible involvement of ATP-sensitive K channels were examined with cultured rat hippocampal neurons. The results and conclusions are as follows.
1.The ischemia induced the suppression of the synaptic transmission. The inhibitory transmission was more fragile than the excitatory transmission.
2.ATP-sensitive K channels were not involved in the ischemia-induced suppression of the transmission, but contributed to the recovery from it.
3.Ca-dependent K channels at the presynaptic terminals did not contribute to the modulation of the synaptic transmission (Neurosci.Lett.207 : 195-198).
4.Both the excitatory and the inhibitory transmissions were modulated by the activation of metabotropic glutamate receptors at the presynaptic terminals (Brain Res.705 : 337-340). Thus, it seems likely that the ischemia induces an increase in external glutamate concentration, which in turn modulates the synaptic transmissions.
5.The depolarization of postsynaptic neurons induced the suppression of the inhibitory transmission, via the retrograde signaling (submitted). Thus, it seems possible that the ischemia induced the depolarization of neurons, which in turn suppresses the inhibitory transmission.
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