Propofol prevents electroconvulsive-shock-induced memory impairment through regulation of hippocampal synaptic plasticity in a rat model of depression.

摘要: Background Although a rapid and efficient psychiatric treatment, electroconvulsive therapy (ECT) induces memory impairment. Modified ECT requires anesthesia for safety purposes. traditionally found to exert amnesic effects in general anesthesia, which is an inherent part of modified ECT, some anesthetics have been protect against ECT-induced cognitive However, the mechanisms remain unclear. We investigated propofol (2,6-diisopropylphenol) on depressed rats undergoing shock (ECS), analog animals, under as well its mechanisms. Methods Chronic unpredictable mild stresses were adopted reproduce depression rodent model. Rats underwent ECS (or sham ECS) with or normal saline. Behavior was assessed sucrose preference, open field Morris water maze tests. Hippocampal long-term potentiation (LTP) measured using electrophysiological techniques. PSD-95, CREB, p-CREB protein expression assayed Western blotting. Results Depression induced damage, downregulated LTP, p-CREB; these exacerbated by ECS; did not reverse depression-induced changes, but when administered ECS, improved reversed downregulation LTP proteins. Conclusion These findings suggest that prevents ECS-induced impairment, improves rats, possibly reversing excessive changes hippocampal synaptic plasticity. observations provide novel insight into potential targets optimizing clinical use disorders.