Department of Neuropsychiatry, Nippon Medical School, Tokyo, Japan.
Int J Neuropsychopharmacol. 2010 Jul;13(6):785-91. doi: 10.1017/S1461145709991209. Epub 2010 Jan 13.
In our previous positron emission tomography (PET) study, we demonstrated that ECT decreased dopamine D2 receptor in major depressive disorder (MDD). Although many animal studies have focused on the effect of ECT on serotonergic neurotransmission, no human study has directly examined the effect of ECT on brain serotonin [5-hydroxytryptamine (5-HT)] 1A receptors (5-HT1ARs). Using PET with [11C]WAY 100635, we aimed to evaluate the effect of ECT on 5-HT1ARs in patients with MDD. Nine patients underwent PET scans before and after a series of 6-7 bilateral ECTs. Region-of-interest analysis was performed based on the simplified reference tissue model. There were no significant changes in 5-HT1AR binding in patients between before and after ECT. ECT did not alter [11C]WAY 100635 binding even after recovery from depressive episode. Although the present finding does not exclude the involvement of brain 5-HT1A systems in the antidepressant action of ECT, it may indicate the involvement of other neurotransmission mechanisms.
在我们之前的正电子发射断层扫描（PET）研究中，我们证明了电抽搐治疗（ECT）会降低重度抑郁症（MDD）患者的多巴胺 D2 受体。尽管许多动物研究都集中在 ECT 对 5-羟色胺能神经传递的影响上，但没有人类研究直接检查 ECT 对大脑 5-羟色胺[5-羟色胺（5-HT）]1A 受体（5-HT1AR）的影响。我们使用 [11C]WAY 100635 的 PET 来评估 ECT 对 MDD 患者 5-HT1AR 的影响。9 名患者在一系列 6-7 次双侧 ECT 前后接受了 PET 扫描。根据简化参考组织模型进行了感兴趣区域分析。ECT 前后患者的 5-HT1AR 结合没有明显变化。即使在抑郁发作缓解后，ECT 也不会改变 [11C]WAY 100635 的结合。虽然目前的发现不能排除脑 5-HT1A 系统在 ECT 抗抑郁作用中的参与，但它可能表明其他神经传递机制的参与。
