1997 Fiscal Year Final Research Report Summary
THE ROLE OF G PROTEIN-COUPLED RECEPTOR AND EFFECTOR IN THE BASIC MECHANISMS IN EP ILEPSY
| Project/Area Number |
08457248
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | CHIBA UNIVERSITY |
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Principal Investigator |
IWASA Hiroto CHIBA UNIVERSITY SCHOOL OF MEDICINE,Lecturer, 医学部, 講師 (60203361)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Athuhiro CHIBA UNIVERSITY SCHOOL OF MEDICINE,Assistant, 医学部, 助手 (60272332)
HASEGAWA Shuji CHIBA CITY INSTITUTE OF HEALTH AND ENVIRONMENT,Chief, 所長
KIKUCHI Shuichi Natinal Institute of Mental Health, Chief Rsearcher, 精神保健研究所, 主任研究員
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| Project Period (FY) |
1996 – 1997
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| Keywords | G proteins / Epilepsy / Kindling / Adenylate cyclase / Hippocampus / Gs / beta-adrenargic receptor / in situ hybridization |
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| Research Abstract |
In the present study, we examined the mRNA expression levels of adenylate cyclase II (ACII) and Gs alpha using the northern blot method in the hippocampus of amygdaloid kindled rats and also examined the changes of beta (beta1, beta2) -adrenargic receptor by in situ hybridization. The ACII mRNA level was increased significantly on both sides of the hippocampus at 24 hours after the last class 5 generalized seizure while the Gs alpha mRNA level was unaltered. Significant increase in Gs alpha mRNA expression level was observed on the stimulated side of the hippocampus and beta- adrenargic receptor mRNA level were increased remarkably in the bilateral dentate gyrus at 3 weeks after the last generalized seizure while the ACII mRNA level exhibited only a slight increase. There were no changes in expression levels of Gsalpha, beta-adrenargic receptor and ACII mRNAs in the sham-stimulated and partially-kindled rats. These results suggest that increases of the mRNA expression levels of beta-adrenargic receptor, ACII and Gsalpha might have an impact on the basic mechanisms of seizure generation and maintenance of persistent increase of seizure susceptibility rather than in the acquisition process of epileptogenesis.
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