Tunca Zeliha, Bayn Mehmet, Alkn Tunç, Özerdem Ayşegül, Resmi Halil, Akan Pnar
From the *Department of Psychiatry, School of Medicine, Dokuz Eylül University, Izmir, Turkey; and †Private Hospital, Nevşehir, Turkey.
J ECT. 2015 Sep;31(3):167-72. doi: 10.1097/YCT.0000000000000198.
Neurotrophic factors are known to be involved in the pathogenesis of mood disorders. However, the precise neurobiology underlying relapse into depression or switch to mania under antidepressant treatment is not fully understood. Evidence suggests the role of neuroplasticity in these processes.
Brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor (GDNF) serum levels were measured concomitantly during electroconvulsive treatment (ECT) in 30 depressive patients (25 patients with unipolar, 5 with bipolar depression), including those who relapsed into depression (n = 6) or switched to mania (n = 3) within 1 to 4 weeks after the end of the ECT, and in 33 healthy volunteers.
Despite significant decrease in depression scores, the levels of brain-derived neurotrophic factor did not significantly change during the ECT, also in the patients who relapsed into depression or switched to mania. However, GDNF levels were lower in the ECT responders compared with pre-ECT levels (z = -2.203; P = 0.01) and increased in manic switch compared with the ECT responders (z = -2.761; P = 0.001) (Cohen d = -1.75; effect size r = -0.66) and healthy controls as well (P = 0.044).
Our data suggest the role of GDNF in manic switch and the involvement of glial system in the pathogenesis of mood disorders.
已知神经营养因子参与情绪障碍的发病机制。然而，抗抑郁治疗后复发为抑郁或转为躁狂的确切神经生物学机制尚未完全明确。有证据表明神经可塑性在这些过程中发挥作用。
在30例抑郁症患者（25例单相抑郁患者，5例双相抑郁患者）接受电休克治疗（ECT）期间，同时检测其脑源性神经营养因子和胶质细胞源性神经营养因子（GDNF）的血清水平，这些患者包括在ECT结束后1至4周内复发为抑郁（n = 6）或转为躁狂（n = 3）的患者，另外选取33名健康志愿者作为对照。
尽管抑郁评分显著降低，但在ECT期间，脑源性神经营养因子水平并未显著变化，复发为抑郁或转为躁狂的患者亦是如此。然而，ECT有效者的GDNF水平较ECT前降低（z = -2.203；P = 0.01），转为躁狂者的GDNF水平较ECT有效者升高（z = -2.761；P = 0.001）（Cohen d = -1.75；效应量r = -0.66），且与健康对照组相比也有升高（P = 0.044）。
我们的数据表明GDNF在躁狂转换中发挥作用，且胶质细胞系统参与情绪障碍的发病机制。
