1999 Fiscal Year Final Research Report Summary
Slow potentiation of CaィイD12+ィエD1-dependent depolarizing spike afterdepdarization in pyramidal, cells.
| Project/Area Number |
10680765
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
KANG Youngnam Kyoto University, Physiology, associate Professor, 医学研究科, 助教授 (50177755)
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| Project Period (FY) |
1998 – 1999
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| Keywords | memory. learning / r-band EEG / fast rhythmic burst / Calcium dependency / depolarizing afterpotentials / Cerebral cortex / cationic current / Pyramidal cell |
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| Research Abstract |
Regular spiking pattern in some pyramidal cells has been demonstrated to be changed into fast rhythmic bursting pattern. Fast rhythmic bursting neurons are presumed to play a crucial role in evoking gamma-band EEG oscillation that is observed on cognition or on rehearsal of short term memory. Since the enhancement of depolarizing afterpotentials (DAP) appeared to be involved in the transformation of firing pattern, we investigated the ionic mechanisms underlying the DAP and its potentiation in pyramidal cells in rat frontal cortical slices using the whole-cell recording method. The generation of DAP was found to be mediated by a Ca2+ dependent cationic current which can be expressed as a slow tail current (I),lasting for a few seconds after the offset of depolarization pulses under voltage clamp conditions. Slow tail-Is were prolonged by bath application of caffeine (10 mM). Repetitive application of depolarizing pulses in the presence of caffeine led to a generation of a much slower tail-I lasting for a few tens of seconds. Simultaneous measurements of tail current and fluorescent ratio revealed that the Ca2+ sensitivity of the cationic channel is upregulated after a transient increase in [Ca2+]i. KN-62 and KN-93, inhibitors of CaM KII, suppressed this enhancement of slow tail-Is without affecting CICR, indicating that activation of CaM KII may play a crucial role in the upregulation of Ca2+ dependent cationic channels. It was suggested that the generation of slower tail-I in the presence of caffeine was largely dependent on the transient increase in [Ca2+]i. The increased Ca2+ may in turn activate CaM KII to phosphorylate cationic channels. This would be consistent with our previous observation that repetitive application of strong depolarization induced fast rhythmic burst firing as a consequence of an enhancement of DAP.
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