CaV2.1 (P/Q-type) and CaV2.2 (N-type) voltage-gated Ca2+ channels play pivotal roles in synaptic transmission and neuroendocrine hormone secretion by coupling excitation (i.e. action potential firing) to transmitter release through Ca2+-dependent exocytosis. Consequently, multiple protein-protein interactions and cell signaling pathways converge on these channels to precisely control the amount, location, and timing of Ca2+ entry. Among these, G protein coupled receptors (GPCRs) respond to autocrine, paracrine, and retrograde chemical signals to provide important feedback regulation. Several distinct signaling pathways recruited by GPCRs can converge on Ca2+ channels, however this chapter focuses on the so-called voltage-dependent inhibition mediated by direct binding of G protein βγ subunits (Gβγ) to the channels. This includes an overview of the functional impact of Gβγ on CaV2 channels and current understanding of the molecular mechanisms involved. Neuroendocrine chromaffin cells are also highlighted as both a physiologically important system and powerful cellular model to investigate modulation of Ca2+ channels and neurosecretion by GPCRs.
|Original language||English (US)|
|Title of host publication||Modulation of Presynaptic Calcium Channels|
|Number of pages||30|
|ISBN (Print)||9400763336, 9789400763333|
|State||Published - Dec 1 2012|
All Science Journal Classification (ASJC) codes