Carpentier P, Lambrinidis M, Blanchet G
Centre de Recherches, Unité de Neurotoxicologie, La Tronche, France.
Brain Res. 1991 Feb 15;541(2):293-9. doi: 10.1016/0006-8993(91)91030-5.
In rats poisoned with soman (s.c. 100 micrograms/kg), a potent inhibitor of cholinesterase (ChE), the numbers of dendritic spines of Golgi impregnated hippocampal pyramidal cells (CA1 sector) were evaluated within the first hour of the intoxication. Animals that experienced convulsions showed a rapid and striking decrease in the density of dendritic spines which could be reduced by nearly 80% of the controls in the basal dendrites 60 min post-soman exposure. Although the exact mechanisms cannot be determined from the present study, it is suggested that the spine loss may represent: (1) the first sign of the seizure-related neuronal changes which are known to occur later during soman intoxication; and (2) the expression of the 'dendrotoxic' effects produced by certain non-cholinergic excitatory transmitters such as glutamate.
在被梭曼（皮下注射100微克/千克）中毒的大鼠中，梭曼是一种强效胆碱酯酶（ChE）抑制剂，在中毒后的第一小时内评估了高尔基染色的海马锥体细胞（CA1区）树突棘的数量。经历惊厥的动物树突棘密度迅速且显著降低，在接触梭曼60分钟后，基底树突中的树突棘密度可降至对照组的近80%。尽管从本研究中无法确定确切机制，但有人认为树突棘丧失可能代表：（1）癫痫相关神经元变化的首个迹象，已知这种变化在梭曼中毒后期会出现；（2）某些非胆碱能兴奋性递质如谷氨酸产生的“树突毒性”效应的表现。
