NITRIC-OXIDE - AN ENDOGENOUS ANTICONVULSANT SUBSTANCE
NITRIC-OXIDE - AN ENDOGENOUS ANTICONVULSANT SUBSTANCE
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DOI：
10.1097/00001756-199304000-00027
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发表时间：
1993-04-01
期刊：
影响因子：
1.7
通讯作者：
BOULU, RG
中科院分区：
文献类型：
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作者：
BUISSON, A;LAKHMECHE, N;BOULU, RG
在本研究中，我们研究了 L-精氨酸-一氧化氮途径在癫痫发作活动终止中的参与。通过向清醒小鼠脑室内注射 N-甲基-D-天冬氨酸可重复诱导惊厥。通过抑制 NO 通路或脑室内注射亚甲蓝（一种鸟苷酸环化酶活性抑制剂）可延长癫痫发作的持续时间。通过同时给予 L-精氨酸或脑室内注射鸟苷 3':5' 环单磷酸 (cGMP)，可以逆转癫痫发作持续时间的延长。这些结果表明，响应 NMDA 受体激活而产生的一氧化氮导致 cGMP 增加，从而诱导癫痫发作活动终止。
IN the present study, we examine the involvement of the L-arginine-nitric oxide pathway in seizure activity termination. Convulsions were induced reproducibly by intracerebroventricular administration of N-methyl-D-aspartate to conscious mice. The duration of the seizure activity was increased by inhibition of the NO-pathway or by intracerebroventricular injection of methylene blue, an inhibitor of guanylate cyclase activity. This increased duration in seizure activity was reversed by co-administration of L-arginine or by intracerebroventricular injection of guanosine 3':5' cyclic monophosphate (cGMP). These results suggest that nitric oxide produced in response to NMDA receptor activation leads to an increase in cGMP which induces the seizure activity termination.