Abstract
In the spinal cord, presynaptic CaV2.2 channels relay sensory input via calcium-induced neurotransmission. CaV2.2 channels can operate in two modes - willing or reluctant - strengthening or weakening transmission, respectively. CaV2.2 channels are composed of a central ion-conducting pore, surrounded by four different voltage-sensing domains (VSDs I-IV). Reluctant gating shifts the CaV2.2 voltage-dependent opening towards positive potentials during neurotransmitter inhibition, via the G-protein complex Gβγ. Gβγ directly inhibits CaV2.2 channels and the interaction can be relieved by a depolarizing prepulse. We hypothesize that Gβγ-induced reluctant gating involves the modification of one or more CaV2.2 VSD(s).
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