L-type calcium channels in exocytosis and endocytosis of chromaffin cells

• Published in: Pflügers Archiv 2018, Vol.470 (1), p.53-60
• Main Authors: Nanclares, Carmen, Baraibar, Andrés M., Gandía, Luis
• Format: Article
• Language: English
• Subjects: Action Potentials; Animals; Biomedical and Life Sciences; Biomedicine; Calcium Channel Blockers - pharmacology; Calcium channels; Calcium channels (L-type); Calcium channels (voltage-gated); Calcium Channels, L-Type - metabolism; Calcium influx; Catecholamines; Cell Biology; Channel gating; Chromaffin cells; Chromaffin Cells - drug effects; Chromaffin Cells - metabolism; Chromaffin Cells - physiology; Depolarization; Endocytosis; Exocytosis; Human Physiology; Humans; Invited Review; Molecular Medicine; Neurosciences; Neurotransmitter release; Plasma membranes; Receptors
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s00424-017-2064-1

The coexistence of different subtypes of voltage-dependent calcium channels (VDCC) within the same chromaffin cell (CC) and the marked interspecies variability in the proportion of VDCC subtypes that are present in the plasmalemma of the CCs raises the question on their roles in controlling different physiological functions. Particularly relevant seems to be the role of VDCCs in the regulation of the exocytotic neurotransmitter release process, and its tightly coupled membrane retrieval (endocytosis) process since both are Ca 2+ -dependent processes. This review is focused on the role of Ca 2+ influx through L-type VDCC in the regulation of these two processes. It is currently accepted that the different VDCC subtypes (i.e., T, L, N, P/Q, R) contribute to exocytosis proportionally to their density of expression and gating properties. However, the pattern of stimulation defines a preferential role of the different subtypes of VDCC on exocytosis and endocytosis. Thus, L-type channels seem to control catecholamine release induced by prolonged stimuli while fast exocytosis in response to short square depolarizing pulses or action potentials is mediated by Ca 2+ entering CCs through P/Q channels. The pattern of stimulation also influences the endocytotic process, and thus, electrophysiological data suggest the sustained Ca 2+ entry through slow-inactivating L-type channels could be responsible for the activation of fast endocytosis.