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자료유형
학술저널
저자정보
Koh, Jun-Seok (Department of Neurosurgery, Hospital of Kyung-Hee University College of Medicine) Kim, Gook-Ki (Department of Neurosurgery, Hospital of Kyung-Hee University College of Medicine) Lim, Young-Jin (Department of Neurosurgery, Hospital of Kyung-Hee University College of Medicine) Rhee, Bong-Arm (Department of Neurosurgery, Hospital of Kyung-Hee University College of Medicine) Kim, Tae-Sung (Department of Neurosurgery, Hospital of Kyung-Hee University College of Medicine)
저널정보
대한신경외과학회 대한신경외과학회지 대한신경외과학회지 제38권 제4호
발행연도
2005.1
수록면
287 - 292 (6page)

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Objective : Kainic acid[KA] enhances the expression of nitric oxide synthase, increases nitric oxide[NO], and thus evokes epileptic convulsion, which results in neuronal damage in the rat brain. NO may stimulate cyclooxygenase type-2 [COX-2] activity, thus producing seizure and neuronal injury, but it has also been reported that KA-induced seizure and neurodegeneration are aggravated on decreasing the COX-2 level. This study was undertaken to investigate whether the suppression of NO using the NOS inhibitor, N-nitro-L-arginine methyl ester[L-NAME], suppresses or enhances the activity of COX-2. Methods : Silver impregnation and COX-2 immunohistochemical staining were used to localize related pathophysiological processes in the rat forebrain following KA-induced epileptic convulsion and L-NAME pretreatment. Post-injection survival of the rat was 1, 2, 3days and 2months, respectively. Results : After the systemic administration of KA in rats, neurodegeneration increased with time in the cornu ammonis [CA] 3, CA 1 and amygdala, as confirmed by silver impregnation. On pretreating L-NAME, KA-induced neuronal degeneration decreased. COX-2 enzyme activities increased after KA injection in the dentate gyrus, CA 3, CA 1, amygdala and pyriform cortex, as determined by COX-2 staining. L-NAME pretreatment prior to KA-injection, caused COX-2 activities to increase compared with KA- injection only group by 1day and 2days survival time point. Conclusion : These results suggest that L-NAME has a neuroprotective effect on KA-induced neuronal damage, especially during the early stage of neurodegeneration.

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