Kamp M A, Krieger A, Henry M, Hescheler J, Weiergräber M, Schneider T
Institute of Neurophysiology, Robert-Koch-Str. 39, D-50931 Köln, Germany.
Eur J Neurosci. 2005 Mar;21(6):1617-25. doi: 10.1111/j.1460-9568.2005.03984.x.
Ca2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis. Within the group of ten cloned voltage-gated Ca2+ channels, the Ca(v)2.3-containing E-type Ca2+ channels are involved in various physiological processes, such as neurotransmitter release and exocytosis together with other voltage-gated Ca2+ channels of the Ca(v)1, Ca(v)2 and Ca(v)3 subfamily. However, E-type Ca2+ channels also exhibit several subunit-specific features, most of which still remain poorly understood. Ca(v)2.3-containing R-type channels (here called 'E-type channels') are also located in presynaptic terminals and interact with some synaptic vesicle proteins, the so-called SNARE proteins, although lacking the classical synprint interaction site. E-type channels trigger exocytosis and are also involved in long-term potentiation. Recently, it was shown that the interaction of Ca(v)2.3 with the EF-hand motif containing protein EFHC1 is involved in the aetiology and pathogenesis of juvenile myoclonic epilepsy.
钙离子流入可兴奋细胞是神经递质释放和调节性胞吐作用的前提条件。在十个克隆的电压门控钙离子通道组中,含有Ca(v)2.3的E型钙离子通道参与各种生理过程,如神经递质释放和胞吐作用,同时还有Ca(v)1、Ca(v)2和Ca(v)3亚家族的其他电压门控钙离子通道。然而,E型钙离子通道也表现出几个亚基特异性特征,其中大多数仍了解甚少。含有Ca(v)2.3的R型通道(这里称为“E型通道”)也位于突触前末端,并与一些突触囊泡蛋白(即所谓的SNARE蛋白)相互作用,尽管缺乏经典的突触印记相互作用位点。E型通道触发胞吐作用,也参与长时程增强。最近的研究表明,Ca(v)2.3与含有EF手基序的蛋白EFHC1的相互作用与青少年肌阵挛性癫痫的病因和发病机制有关。