Department of Psychological Medicine, King's College London, London, UK.
J Psychopharmacol. 2020 Oct;34(10):1086-1097. doi: 10.1177/0269881120936538. Epub 2020 Jul 10.
Electroconvulsive therapy (ECT) is a powerful and fast-acting anti-depressant strategy, often used in treatment-resistant patients. In turn, patients with treatment-resistant depression often present an increased inflammatory response. The impact of ECT on several pathophysiological mechanisms of depression has been investigated, with a focus which has largely been on cellular and synaptic plasticity. Although changes in the immune system are known to influence neurogenesis, these processes have principally been explored independently from each other in the context of ECT.
The aim of this review was to compare the time-dependent consequences of acute and chronic ECT on concomitant innate immune system and neurogenesis-related outcomes measured in the central nervous system in pre-clinical studies.
During the few hours following acute electroconvulsive shock (ECS), the expression of the astrocytic reactivity marker glial fibrillary acidic protein (GFAP) and inflammatory genes, such as cyclooxygenase-2 (COX2), were significantly increased together with the neurogenic brain-derived neurotrophic factor (BDNF) and cell proliferation. Similarly, chronic ECS caused an initial upregulation of the same astrocytic marker, immune genes, and neurogenic factors. Interestingly, over time, inflammation appeared to be dampened, while glial activation and neurogenesis were maintained, after either acute or chronic ECS.
Regardless of treatment duration ECS would seemingly trigger a rapid increase in inflammatory molecules, dampened over time, as well as a long-lasting activation of astrocytes and production of growth and neurotrophic factors, leading to cell proliferation. This suggests that both innate immune system response and neurogenesis might contribute to the efficacy of ECT.
电痉挛疗法（ECT）是一种强大且快速起效的抗抑郁策略，常用于治疗抵抗的患者。反过来，治疗抵抗的抑郁症患者通常表现出更高的炎症反应。ECT 对抑郁症的几个病理生理机制的影响已经得到了研究，研究重点主要集中在细胞和突触可塑性上。尽管免疫系统的变化已知会影响神经发生，但这些过程在 ECT 的背景下主要是彼此独立地进行探索的。
本综述的目的是比较急性和慢性 ECT 对中枢神经系统中同时测量的固有免疫系统和神经发生相关结果的时间依赖性影响，这些结果是在临床前研究中得到的。
在急性电抽搐（ECS）后的几个小时内，星形胶质细胞反应标志物胶质纤维酸性蛋白（GFAP）和炎症基因，如环氧化酶-2（COX2）的表达显著增加，同时还伴随着神经发生的脑源性神经营养因子（BDNF）和细胞增殖。同样，慢性 ECS 导致相同的星形胶质细胞标志物、免疫基因和神经发生因子的初始上调。有趣的是，随着时间的推移，炎症似乎被抑制，而在急性或慢性 ECS 后，胶质细胞激活和神经发生都得到维持。
无论治疗持续时间如何，ECS 似乎都会引发炎症分子的快速增加，随着时间的推移而减弱，同时还会引发星形胶质细胞的长期激活和生长和神经营养因子的产生，从而导致细胞增殖。这表明固有免疫系统反应和神经发生都可能有助于 ECT 的疗效。
