Abstract

The review discusses molecular and cellular mechanisms common to the temporal lobe epileptogenesis/epilepsy and depressive disorders. Comorbid temporal lobe epilepsy and depression are associated with dysfunction of the hypothalamic-pituitary-adrenocortical axis. Excessive glucocorticoids disrupt the function and impair the structure of the hippocampus, a brain region key to learning, memory, and emotions. Selective vulnerability of the hippocampus to stress, mediated by the reception of glucocorticoid hormones secreted during stress, is the price of the high functional plasticity and pleiotropy of this limbic structure. Common molecular and cellular mechanisms include the dysfunction of glucocorticoid receptors, neurotransmitters, and neurotrophic factors, development of neuroinflammation, leading to neurodegeneration and loss of hippocampal neurons, as well as disturbances in neurogenesis in the subgranular neurogenic niche and formation of aberrant neural networks. These glucocorticoid-dependent processes underlie altered stress response and the development of chronic stress-induced comorbid pathologies, in particular, temporal lobe epilepsy and depressive disorders.

中文翻译：

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癫痫和共病性抑郁症常见的应激相关分子和细胞海马机制

摘要

该评论讨论了颞叶癫痫发生/癫痫和抑郁症共有的分子和细胞机制。合并性颞叶癫痫和抑郁症与下丘脑-垂体-肾上腺皮质轴功能障碍有关。过量的糖皮质激素会破坏海马的功能并损害海马的结构，海马是学习，记忆和情绪的关键大脑区域。由应激过程中分泌的糖皮质激素的接受介导的海马对应激的选择性脆弱性是这种边缘结构的高功能可塑性和多效性的代价。常见的分子和细胞机制包括糖皮质激素受体，神经递质和神经营养因子的功能障碍，神经炎症的发展，导致神经变性和海马神经元丢失，以及亚颗粒下神经源性利基神经元生成的异常和异常神经网络的形成。这些糖皮质激素依赖性过程是应激反应改变和慢性应激诱发的合并症（尤其是颞叶癫痫和抑郁症）发展的基础。