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癫痫相关的海马体兴奋性改变。

Epilepsy-associated alterations in hippocampal excitability.

作者信息

Navidhamidi Mojdeh, Ghasemi Maedeh, Mehranfard Nasrin

出版信息

Rev Neurosci. 2017 Apr 1;28(3):307-334. doi: 10.1515/revneuro-2016-0059.

DOI:10.1515/revneuro-2016-0059
PMID:28099137
Abstract

The hippocampus exhibits a wide range of epilepsy-related abnormalities and is situated in the mesial temporal lobe, where limbic seizures begin. These abnormalities could affect membrane excitability and lead to overstimulation of neurons. Multiple overlapping processes refer to neural homeostatic responses develop in neurons that work together to restore neuronal firing rates to control levels. Nevertheless, homeostatic mechanisms are unable to restore normal neuronal excitability, and the epileptic hippocampus becomes hyperexcitable or hypoexcitable. Studies show that there is hyperexcitability even before starting recurrent spontaneous seizures, suggesting although hippocampal hyperexcitability may contribute to epileptogenesis, it alone is insufficient to produce epileptic seizures. This supports the concept that the hippocampus is not the only substrate for limbic seizure onset, and a broader hyperexcitable limbic structure may contribute to temporal lobe epilepsy (TLE) seizures. Nevertheless, seizures also occur in conditions where the hippocampus shows a hypoexcitable phenotype. Since TLE seizures most often originate in the hippocampus, it could therefore be assumed that both hippocampal hypoexcitability and hyperexcitability are undesirable states that make the epileptic hippocampal network less stable and may, under certain conditions, trigger seizures.

摘要

海马体表现出广泛的与癫痫相关的异常,位于内侧颞叶,边缘性癫痫发作起始于此。这些异常可能影响膜兴奋性并导致神经元过度刺激。多个重叠过程指的是神经元中发展出的神经稳态反应,它们共同作用以将神经元放电率恢复到控制水平。然而,稳态机制无法恢复正常的神经元兴奋性,癫痫性海马体变得过度兴奋或兴奋不足。研究表明,在开始反复自发性癫痫发作之前就存在过度兴奋,这表明尽管海马体过度兴奋可能促成癫痫发生,但仅靠它不足以引发癫痫发作。这支持了海马体不是边缘性癫痫发作的唯一底物这一概念,更广泛的过度兴奋的边缘结构可能导致颞叶癫痫(TLE)发作。然而,在海马体表现出兴奋不足表型的情况下也会发生癫痫发作。由于TLE发作最常起源于海马体,因此可以假定海马体兴奋不足和过度兴奋都是不良状态,会使癫痫性海马网络稳定性降低,并可能在某些情况下引发癫痫发作。

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