Naylor P, Stewart C A, Wright S R, Pearson R C, Reid I C
Department of Psychiatry, University of Sheffield, UK.
Brain Res Mol Brain Res. 1996 Jan;35(1-2):349-53. doi: 10.1016/0169-328x(95)00264-s.
The neural basis underlying the cognitive side effects of ECT is unknown. Recent studies suggest that the memory dysfunction may be caused by alterations in hippocampal synaptic efficacy [20]. In situ hybridisation was used to examine the possible receptor mechanisms responsible for this effect. Repeated ECS markedly increased mRNA expression for the GluR1 subunit of the AMPA receptor, but not the NMDAR1A-G subtypes of the NMDA receptor, relative to control treatments. This effect was present 24 h after the last seizure and may be responsible for the expression of the ECS-induced increase in synaptic efficacy.
ECT认知副作用背后的神经基础尚不清楚。最近的研究表明，记忆功能障碍可能是由海马体突触效能的改变引起的[20]。采用原位杂交技术来检测导致这种效应的可能受体机制。相对于对照处理，反复进行电惊厥休克（ECS）显著增加了AMPA受体GluR1亚基的mRNA表达，但未增加NMDA受体的NMDAR1A-G亚型的mRNA表达。这种效应在最后一次癫痫发作后24小时出现，可能是ECS诱导的突触效能增加得以表达的原因。
