Project/Area Number |
16591145
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Psychiatric science
|
Research Institution | University of Miyazaki |
Principal Investigator |
ISHIDA Yasushi University of Miyazaki, Faculty of Medicine, Professor, 医学部, 教授 (20212897)
|
Co-Investigator(Kenkyū-buntansha) |
UEDA Yuto University of Miyazaki, Faculty of Medicine, Associate Professor, 医学部, 助教授 (70244192)
ABE Hiroshi University of Miyazaki, Faculty of Medicine, Assistant, 医学部, 助手 (20344848)
NISHIMORI Toshikazu University of Miyazaki, Faculty of Medicine, Professor, 医学部, 教授 (20112211)
TAKEDA Ryuichiro University of Miyazaki, Faculty of Medicine, Assistant, 医学部, 助手 (90336298)
|
Project Period (FY) |
2004 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
Keywords | audiogenic seizure / GABA / glutamate receptor / c-Fos / immunohistochemistry / rat / 聴覚誘発痙攣 / 強直間代発作 / 疾走発作 |
Research Abstract |
Given the evidence that the inferior colliculus (IC) and superior colliculus (SC) seem to play key roles in connecting auditory pathways and seizure output pathways in the neuronal network for audiogenic seizures (AS) in rats, we examined Fos activation in GABAergic cells and cells immunopositive for glutamate N-methyl-D-aspartate (NMDA) receptors in the IC and SC following AS using the double-labeling procedure. Generalized tonic-clonic seizures (GTCS), which developed as an advanced form of AS in some of the susceptible rats, induced an increase in Fos expression in three IC substructures-the dorsal cortex of IC (DCIC), central nucleus of IC (CIC), and external cortex of IC (ECIC)-and in one SC substructure-the deep gray layer of SC (DpG). Compared with the rats showing GTCS, rats exhibiting wild running (WR) without proceeding to GTCS showed a different pattern of AS-induced Fos expression. The DpG in the WR animals showed no significant increase in the levels of Fos-like immunoreactivity. The degrees of Fos activation that occurred in GABAergic cells and cells immunopositive for NMDA receptors were similar in the DCIC, CIC, ECIC, and DpG following AS. These results suggest that Fos activation in the DpG is involved in the development from WR to GTCS in AS-susceptible rats. They also provide some evidence that some GABAergic neurons in the IC and SC and glutamatergic afferents (via NMDA receptors) to these structures are activated by AS.
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