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Presynaptic ‘Cav2.3‐containing’ E‐type Ca2+ channels share dual roles during neurotransmitter release

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AbstractCa2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis. Within the group of ten cloned voltage‐gated Ca2+ channels, the Cav2.3‐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 Cav1, Cav2 and Cav3 subfamily. However, E‐type Ca2+ channels also exhibit several subunit‐specific features, most of which still remain poorly understood. Cav2.3‐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 Cav2.3 with the EF‐hand motif containing protein EFHC1 is involved in the aetiology and pathogenesis of juvenile myoclonic epilepsy.
Title: Presynaptic ‘Cav2.3‐containing’ E‐type Ca2+ channels share dual roles during neurotransmitter release
Description:
AbstractCa2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis.
Within the group of ten cloned voltage‐gated Ca2+ channels, the Cav2.
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 Cav1, Cav2 and Cav3 subfamily.
However, E‐type Ca2+ channels also exhibit several subunit‐specific features, most of which still remain poorly understood.
Cav2.
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 Cav2.
3 with the EF‐hand motif containing protein EFHC1 is involved in the aetiology and pathogenesis of juvenile myoclonic epilepsy.

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