1996 Fiscal Year Final Research Report Summary
Experimental analysis of behavior of Fyn-deficient mice
| Project/Area Number |
07451018
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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 |
実験系心理学
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| Research Institution | Univ. of Tokyo |
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Principal Investigator |
NIKI Hiroaki Univ. of Tokyo Dept. of Psychology, Graduate Sch. of Humanities & Sociology, Prof, 大学院・人文社会系研究科, 教授 (10073074)
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| Co-Investigator(Kenkyū-buntansha) |
YAGI Takeshi Univ. of Tokyo Lab. of Neurobiol., National Institute of Physiol. Sciences, Inst, 生理学研究所, 助手 (10241241)
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| Project Period (FY) |
1995 – 1996
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| Keywords | gene targeting / Fyn-deficient mice / seizure / metrazol / bicuculline / picrotoxin / kainic acid / NMDA |
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| Research Abstract |
Fyn protein is one of the non-receptor type tyrosine kinases of the Src family and is strongly expressed in the brain. Mice deficient for the fyn gene were examined for their susceptibility to acoustically primed audiogenic seizures and seizures induced by various convulsive drugs, including mertrazol, picrotoxin, bicuculline, kainic acid, NMDA and strychnine. Homozygous mutant (fynz/fynz) mice were significantly more susceptible to audiogenic seizures. They were also more likely to show myoclonic convulsions than were heterozygous mutants (+/fynz) when metrazol, picrotoxin, bicuculline, kanic acid and NMDA were administered. On the other hand, no difference in seizure susceptibility was found between homozygous and heterozygous mutants when strychnine was administered. These results suggest a role of Fyn in seizures induced by loud acoustic stimulus and by convulsive drugs (anti-GABAeregic and glutamic/aspatic acid excitatory receptor agonists).
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