Evidence from lesion studies for epileptogenic and non-epileptogenic neurotoxic interactions between kainic acid and excitatory innervation.
Evidence from lesion studies for epileptogenic and non-epileptogenic neurotoxic interactions between kainic acid and excitatory innervation.
复制标题
红藻氨酸与兴奋性神经支配之间致癫痫和非致癫痫神经毒性相互作用的病变研究证据。
DOI：
10.1016/0006-8993(81)90351-6
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发表时间：
1981
期刊：
影响因子：
2.9
通讯作者：
Smith,EM
中科院分区：
文献类型：
--
作者：
Nadler,JV;Evenson,DA;Smith,EM
kainic酸对大鼠海马神经元的毒性取决于特定兴奋性传入事件的存在。关键通路的急性破坏基本上消除了脑室内kainic酸的神经毒性，但部分或全部海马神经元继续被局部注射kainic酸破坏，直到关键通路退化。这些结果支持了kainic酸通过两种方式破坏海马神经元的观点：(1)通过启动致死性癫痫持续状态；(2)通过与某些通路相互作用，而不依赖于这些通路内正在进行的电活动。
The toxicity of kainic acid toward rat hippocampal neurons depends on the presence of specific excitatory afferents. Acute destruction of the critical pathway essentially abolishes the neurotoxicity of intraventricular kainic acid, but some or all hippocampal neurons continue to be destroyed by locally-injected kainic acid until the critical pathway(s) degenerates. These results support the view that kainic acid destroys hippocampal neurons in two ways: (1) by initiating a lethal status epilepticus; and (2) by interacting with certain pathways independently of on-going electrical activity within those pathways.