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

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

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ＦＳ０．１ｍｇ·ｋｇ－１ｉｍ（ｎ＝２４）或毒扁豆碱３０．０ｍｇ·ｋｇ－１ｉｖ（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＃ＦＳＮ＃ＦＫ受体激动剂烟碱１．０ｍｇ·ｋｇ－１ｉｖ（ｎ＝３８）和中枢Ｍ受体激动剂槟榔碱１５０ｍｇ·ｋｇ－１ｉｖ（ｎ＝４６）或匹鲁卡品３８０ｍｇ·ｋｇ－１ｉｖ（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。

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.