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来自损伤研究的证据表明,海藻酸与兴奋性神经支配之间存在致痫性和非致痫性神经毒性相互作用。

Evidence from lesion studies for epileptogenic and non-epileptogenic neurotoxic interactions between kainic acid and excitatory innervation.

作者信息

Nadler J V, Evenson D A, Smith E M

出版信息

Brain Res. 1981 Feb 2;205(2):405-10. doi: 10.1016/0006-8993(81)90351-6.

Abstract

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.

摘要

海藻酸对大鼠海马神经元的毒性取决于特定兴奋性传入神经的存在。关键通路的急性破坏基本上消除了脑室内注射海藻酸的神经毒性,但一些或所有海马神经元仍会被局部注射的海藻酸破坏,直到关键通路退化。这些结果支持这样一种观点,即海藻酸通过两种方式破坏海马神经元:(1)引发致命的癫痫持续状态;(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。

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