梭曼和毒扁豆碱引起大鼠脑电癫痫波的M和N胆碱能成分

在加拉碘铵麻痹, 人工呼吸维持和甲基阿托品预防的大鼠上, 梭曼0.1 mg·kg^-1 im (n=24)或毒扁豆碱30.0 mg·kg^-1 iv (n=18)使全部大鼠脑电图(EEG)上出现早期持续很短的紧张性癫痫波和随后持续很长的阵挛性癫痫波. 中枢N受体激动剂烟碱1.0 mg·kg^-1 iv (n=38)和中枢M受体激动剂槟榔碱150 mg·kg^-1 iv (n=46)或匹鲁卡品380 mg·kg^-1 iv (n=24)能分别在EEG癫痫波的特征, 出现时间和持续时间上模拟出上述早期紧张性癫痫波和随后的阵挛性癫痫波. 预先小剂量iv烟碱使中枢N受体脱敏或给小剂量N受体拮抗剂美加明保护中枢N受体后, 梭曼只能引起潜伏 期较长且持续很久的阵挛性癫痫波. 胆碱酯酶抑制剂梭曼和毒扁豆碱较大剂量引起大鼠EEG癫痫波可能的机理是过量的乙酰胆碱作用于潜伏期短, 容易脱敏的N受体出现早期持续很短的EEG紧张性癫痫波, 又作用于潜伏期较长, 不容易脱敏的M受体, 出现稍后的EEG阵挛性癫痫波.

Muscarinic and nicotinic components of electroen-cephalogram seizure discharges induced by soman and physostigmine in rats

In gallamine immobilized rats, pre- treated with atropine methyl bromide and maintained under artificial respiration, soman 1.0 mg·kg^-1 im (n=24) or physostigmine 30.0 mg·kg^-1 iv (n=18) produced characteristic electroencephalogram (EEG) patterns shown as initial tonic seizure discharges with short period and subsequent long term clonic seizure discharges. These discharges could be mimicked by N-agonist nicotine 1.0 mg·kg^-1 iv (n=38) and by M-agonists arecoline 150 mg·kg^-1 iv (n=46) or pilocarpine 380 mg·kg^-1 iv (n=24) in all tested rats both in latent period and seizure duration respectively. Pretreatment with repeated iv nicotine, a brain nAChR desensitizer, or with nAChR antagonist mecamylamine iv abolished soman-induced initial EEG tonic discharges but not later EEG clonic discharges. It was suggested that after exposure to anticholinesterase soman or physostigmine, activation of brain nAChR (ion channel gated and easily desensitized) and mAChR (G-protein gated and hardly desensitized) might be responsible for producing initial EEG tonic discharges and subsequent EEG clonic discharges respectively in rats.