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Presynaptic ‘Ca v 2.3‐containing’ E‐type Ca 2+ channels share dual roles during neurotransmitter release
Author(s) -
Kamp M. A.,
Krieger A.,
Henry M.,
Hescheler J.,
Weiergräber M.,
Schneider T.
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.03984.x
Subject(s) - exocytosis , voltage dependent calcium channel , neurotransmitter , synaptic vesicle , active zone , synapsin , neurotransmission , chemistry , microbiology and biotechnology , neuroscience , biophysics , biology , calcium , vesicle , biochemistry , receptor , secretion , membrane , organic chemistry
Ca 2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis. Within the group of ten cloned voltage‐gated Ca 2+ channels, the Ca v 2.3‐containing E‐type Ca 2+ channels are involved in various physiological processes, such as neurotransmitter release and exocytosis together with other voltage‐gated Ca 2+ channels of the Ca v 1, Ca v 2 and Ca v 3 subfamily. However, E‐type Ca 2+ 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.