电压敏感性钙通道（VSCC）拮抗剂ω-阿加毒素-IVA和ω-芋螺毒素-MVIIC可抑制大鼠皮质楔形片中的自发性癫痫样放电。

The voltage-sensitive Ca2+ channel (VSCC) antagonists omega-Aga-IVA and omega-CTX-MVIIC inhibit spontaneous epileptiform discharges in the rat cortical wedge.

作者信息

Robichaud L J, Wurster S, Boxer P A

机构信息

Department of Neuroscience Pharmacology, Parke-Davis Pharmaceutical Research, Division of Warner-Lambert Co., Ann Arbor, MI 48105.

出版信息

Brain Res. 1994 Apr 18;643(1-2):352-6. doi: 10.1016/0006-8993(94)90047-7.

DOI:10.1016/0006-8993(94)90047-7

PMID:8032931

Abstract

The ability of VSCC antagonists to modulate excitatory amino acid (EAA) release was evaluated by measuring N-methyl-D-aspartate (NMDA) receptor-dependent spontaneous epileptiform discharges in rat cortical wedges. The N-type channel blocker omega-CTX-GVIA (300 nM) was ineffective. The P-type channel blocker omega-Aga-IVA at 300 nM reduced the frequency of discharges by 63%, while 300 nM omega-CTX-MVIIC reduced the frequency by 35%. These results coupled with the absence of NMDA antagonism by omega-Aga-IVA or omega-CTX-MVIIC in the cortical wedge suggest that the VSCCs blocked by these toxins are primarily responsible for mediating impulse dependent EAA release in the rat neocortex.

摘要

通过测量大鼠皮质楔形切片中N-甲基-D-天冬氨酸（NMDA）受体依赖性自发性癫痫样放电，评估电压门控性钙通道（VSCC）拮抗剂调节兴奋性氨基酸（EAA）释放的能力。N型通道阻滞剂ω-CTX-GVIA（300 nM）无效。300 nM的P型通道阻滞剂ω-Aga-IVA使放电频率降低了63%，而300 nM的ω-CTX-MVIIC使放电频率降低了35%。这些结果，再加上在皮质楔形切片中ω-Aga-IVA或ω-CTX-MVIIC不存在NMDA拮抗作用，表明被这些毒素阻断的VSCC主要负责介导大鼠新皮质中冲动依赖性EAA的释放。