Institute of Mental Health Research, University of Ottawa, Ottawa, Ontario, K1Z 7K4, Canada.
Synapse. 2013 Oct;67(10):716-27. doi: 10.1002/syn.21685. Epub 2013 Jul 4.
Electroconvulsive therapy (ECT) treats depression by repeated administration of seizure-inducing electrical stimuli. To assess the effects of repeated electroconvulsive shocks (ECSs), an animal model of ECT on monoamine transmission, Sprague-Dawley rats were administered 6 ECS over 2 weeks and in vivo single-unit extracellular electrophysiological recordings were obtained 48 h after the final ECS. Overall firing activity of dopamine (DA) neurons in the ventral tegmental area was unchanged following repeated ECS. In the locus coeruleus (LC), the burst activity of norepinephrine (NE) neurons was increased while population activity was decreased after ECS. In the substantia nigra pars compacta (SNc), there were more spontaneously active neurons, suggesting greater DA tone in the nigrostriatal motor pathway, which may contribute to an alleviation of motor retardation. In the facial motor nucleus (FMN), facilitation of electrophysiological activity by serotonin (5-HT), and NE was determined to be through the 5-HT2C receptor and α1 -adrenoceptor, respectively. Locally administered NE, but not 5-HT, facilitated glutamate-induced firing following repeated ECS, which may contribute to improved motor function. These results showed that repeated ECS enhance DA activity in the SNc and NE transmission in the FMN, which could be a part of the mechanism behind the alleviation of depressive symptoms, including motor retardation, by ECT.
电抽搐治疗(ECT)通过反复给予致痫性电刺激来治疗抑郁症。为了评估重复电休克(ECS)的效果,建立了 ECT 对单胺递质传递影响的动物模型,对 Sprague-Dawley 大鼠给予 6 次 ECS,在最后一次 ECS 后 48 小时进行活体单细胞外电生理记录。重复 ECS 后腹侧被盖区(VTA)多巴胺(DA)神经元的总体放电活动没有变化。在蓝斑核(LC),去甲肾上腺素(NE)神经元的爆发活动增加,而群体活动减少。在黑质致密部(SNc),自发活动神经元增多,提示黑质纹状体运动通路上 DA 张力增加,这可能有助于缓解运动迟缓。在面运动核(FMN),5-羟色胺(5-HT)和 NE 增强电生理活动的作用分别通过 5-HT2C 受体和α1-肾上腺素受体介导。局部给予 NE 而不是 5-HT,可增强重复 ECS 后的谷氨酸诱导放电,这可能有助于改善运动功能。这些结果表明,重复 ECS 增强了 SNc 中的 DA 活性和 FMN 中的 NE 传递,这可能是 ECT 缓解抑郁症状(包括运动迟缓)的机制之一。