2003 Fiscal Year Final Research Report Summary
Genetic research of Epilepsy develops to us treatment.
| Project/Area Number |
13670979
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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 |
Psychiatric science
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| Research Institution | Hirosaki University |
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Principal Investigator |
KURIBAYASHI Michito Hirosaki University, Hospital, Lecture, 医学部附属病院, 講師 (80261436)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Motohiro Hirosaki University, School of Medicine, Lecture, 医学部, 講師 (10281916)
KANEKO Sunao Hirosaki University, School of Medicine, Professor, 医学部, 教授 (40106852)
WADA Kazumaru Hirosaki University, School of Medicine, Professor, 医学部, 教授 (60241486)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Epilepsy / Mood Disorder / Synaptic preotein / Calcium channel / exocytosis / synprint / serotonin / dopamine |
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| Research Abstract |
Entorhinal cortex(EC) is a major source of afferent input to hippocampus via perforant and temporoammonic pathways. We detemined interaction among GABA_A, AMPA/glutamate receptors and protein kinases(PKA and PKC) on exocytosis of GABA and glutamate using multiprobe microdialysis, as well as propagation of neuronal excitability using optical recording in the EC-hippocampal formation. Multiprobe microdialysis demonstrated that EC-evoked GABA release in ventral CA1 was predominantly regulated by PKC-related rather than PKA-related exocytosis mechanism and was augmented by activation of glutamatergic transmission. Contrary to GABA release, EC-evoked glutamate release was predominantly regulated by PKA-related rather than PKC-related mechanisms and was suppressed by activation of GABAergic transmission. Optical recording demonstrated that there are two sub-pathways in temporoammonic pathway, direct projects from EC layers(II-IV) to dendrites on pyramidal cells and GABAergic intemeurons in ventral hippocampal CA1. PKC activation enhanced trisynaptic transmission, in both conditions of GABAA receptor being functional and blocked, whereas PKC activation enhanced and inhibited temporoammonic transmission under conditions of GABAA receptor being functional and blocked, respectively. PKC activation enhanced trisynaptic transmission, in both conditions of being GABAA receptor functional and blockade, whereas PKC activation enhanced and inhibited temporoammonic transmission under conditions of being GABAA receptor functional and blockade, respectively. Thus, GABAergic inhibition, which is regulated by PKC activity, in the temporoammonic pathway is more substantial than that in trisynaptic pathway.
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