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遗传性失神癫痫和急性诱发失神发作的神经化学及行为特征。

Neurochemical and behavioral features in genetic absence epilepsy and in acutely induced absence seizures.

作者信息

Bazyan A S, van Luijtelaar G

机构信息

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Science, Russian Federation, 5A Butlerov Street, Moscow 117485, Russia.

出版信息

ISRN Neurol. 2013 May 7;2013:875834. doi: 10.1155/2013/875834. Print 2013.

DOI:10.1155/2013/875834
PMID:23738145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3664506/
Abstract

The absence epilepsy typical electroencephalographic pattern of sharp spikes and slow waves (SWDs) is considered to be due to an interaction of an initiation site in the cortex and a resonant circuit in the thalamus. The hyperpolarization-activated cyclic nucleotide-gated cationic I h pacemaker channels (HCN) play an important role in the enhanced cortical excitability. The role of thalamic HCN in SWD occurrence is less clear. Absence epilepsy in the WAG/Rij strain is accompanied by deficiency of the activity of dopaminergic system, which weakens the formation of an emotional positive state, causes depression-like symptoms, and counteracts learning and memory processes. It also enhances GABAA receptor activity in the striatum, globus pallidus, and reticular thalamic nucleus, causing a rise of SWD activity in the cortico-thalamo-cortical networks. One of the reasons for the occurrence of absences is that several genes coding of GABAA receptors are mutated. The question arises: what the role of DA receptors is. Two mechanisms that cause an infringement of the function of DA receptors in this genetic absence epilepsy model are proposed.

摘要

失神癫痫典型的脑电图尖峰和慢波（SWDs）模式被认为是由于皮质中的起始位点与丘脑的共振回路相互作用所致。超极化激活的环核苷酸门控阳离子Ih起搏器通道（HCN）在增强皮质兴奋性方面起重要作用。丘脑HCN在SWD发生中的作用尚不清楚。WAG/Rij品系的失神癫痫伴有多巴胺能系统活性不足，这会削弱情绪积极状态的形成，导致类似抑郁的症状，并抵消学习和记忆过程。它还会增强纹状体、苍白球和丘脑网状核中的GABAA受体活性，导致皮质-丘脑-皮质网络中SWD活性升高。失神发作的原因之一是编码GABAA受体的几个基因发生了突变。问题来了：多巴胺受体的作用是什么？本文提出了两种在这种遗传性失神癫痫模型中导致多巴胺受体功能受损的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/e64a035918a7/ISRN.NEUROLOGY2013-875834.011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/bf8284df722e/ISRN.NEUROLOGY2013-875834.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/7ab2c455a2d5/ISRN.NEUROLOGY2013-875834.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/c70926d07756/ISRN.NEUROLOGY2013-875834.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/ed8d1971380a/ISRN.NEUROLOGY2013-875834.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/e229b132f58c/ISRN.NEUROLOGY2013-875834.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/32909490e19c/ISRN.NEUROLOGY2013-875834.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/5f3e577b059b/ISRN.NEUROLOGY2013-875834.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/a195fade79ad/ISRN.NEUROLOGY2013-875834.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/a63170efae56/ISRN.NEUROLOGY2013-875834.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/8f0519146c23/ISRN.NEUROLOGY2013-875834.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c589/3664506/e64a035918a7/ISRN.NEUROLOGY2013-875834.011.jpg

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