Kaneko Takao, Kanazawa Tetsufumi, Nishiguchi Masaki, Kikuyama Hiroki, Tsutsumi Atsushi, Uenishi Hiroyuki, Kawabata Yasuo, Kawashige Seiya, Nishizawa Yoshitaka, Maruyama Souichiro, Koh Jun, Yoneda Hiroshi
From the *Department of Neuropsychiatry, Osaka Medical College, Takatsuki; †Shin-Abuyama Hospital, Takatsuki and ‡Graduate School of Psychology, Kansai University, Suita, Osaka, Japan.
J ECT. 2015 Dec;31(4):234-7. doi: 10.1097/YCT.0000000000000234.
Electroconvulsive therapy (ECT) is currently regarded as a significant treatment option for intractable psychiatric disorders, such as catatonic schizophrenia or treatment-resistant depression; however, the underlying molecular mechanism for its therapeutic effect remains obscure.
Employing microarray analysis (Human Genome U133 Plus 2.0 Array; Affymetrix, United States) of cDNA derived from the peripheral blood of patients with catatonic schizophrenia (n = 5), we detected a significant change in 145 genes (0.68%) before and after modified ECT (mECT). Moreover, we performed quantitative polymerase chain reaction validation of genes that had previously been suggested to be functionally related to schizophrenia.
Of 4 genes examined (AKT3, TCF7, PPP3R1, and GADD45B), only TCF7 was increased during the mECT procedure (P = 0.0025).
This study describes the first attempt to uncover the molecular mechanism of mECT using a microarray assay of mRNA derived from peripheral blood, and our results suggest that the TCF family may play a role in the functional mechanism of mECT.
电休克疗法（ECT）目前被视为治疗顽固性精神疾病的重要选择，如紧张型精神分裂症或难治性抑郁症；然而，其治疗效果的潜在分子机制仍不清楚。
我们采用微阵列分析（人类基因组U133 Plus 2.0芯片；美国Affymetrix公司），对紧张型精神分裂症患者（n = 5）外周血来源的cDNA进行检测，发现在改良电休克疗法（mECT）前后有145个基因（0.68%）发生了显著变化。此外，我们对先前认为与精神分裂症功能相关的基因进行了定量聚合酶链反应验证。
在检测的4个基因（AKT3、TCF7、PPP3R1和GADD45B）中，只有TCF7在mECT治疗过程中表达增加（P = 0.0025）。
本研究首次尝试通过对外周血来源的mRNA进行微阵列分析来揭示mECT的分子机制，我们的结果表明TCF家族可能在mECT的功能机制中发挥作用。
