Berkovic Samuel F, Mulley John C, Scheffer Ingrid E, Petrou Steven
Department of Medicine and Epilepsy Research Centre, University of Melbourne, Austin Health, Heidelberg West, VIC 3081, Australia.
Department of Genetic Medicine, Women's and Children's Hospital and School of Molecular and Biomedical Sciences, University of Adelaide, North Adelaide, SA 5006, Australia.
Trends Neurosci. 2006 Jul;29(7):391-397. doi: 10.1016/j.tins.2006.05.009.
Epilepsies, once regarded as due to demoniacal possession, can have both genetic and acquired causes, with interaction of these factors in many cases. To date, nearly all the genes discovered to be involved in human epilepsies encode subunits of ion channels, both voltage-gated and ligand-gated. Established acquired causes include serious brain trauma, stroke, tumours and infective lesions. Thus, in terms of exploring the neurobiology of "nature and nurture" in disease, the epilepsies are an excellent paradigm. Here, we review the evidence and discuss the possibility that ion channels are a common biological substrate for both genetic and acquired epilepsies. This review is part of the INMED/TINS special issue "Nature and nurture in brain development and neurological disorders", based on presentations at the annual INMED/TINS symposium (http://inmednet.com/).
癫痫曾被认为是由恶魔附身所致，它既有遗传病因，也有后天病因，在许多情况下这两种因素相互作用。迄今为止，几乎所有被发现与人类癫痫相关的基因都编码离子通道亚基，包括电压门控离子通道和配体门控离子通道。已确定的后天病因包括严重脑外伤、中风、肿瘤和感染性病变。因此，在探索疾病中“先天与后天”的神经生物学方面，癫痫是一个极佳的范例。在此，我们综述相关证据，并探讨离子通道作为遗传和后天性癫痫共同生物学基础的可能性。本综述是INMED/TINS特刊“大脑发育与神经疾病中的先天与后天”的一部分，基于在年度INMED/TINS研讨会（http://inmednet.com/）上的报告撰写。
