Electrophysiological and morphological features underlying neurotransmission efficacy at the splanchnic nerve-chromaffin cell synapse of bovine adrenal medulla

Abstract

de Diego AM. Electrophysiological and morphological features underlying neurotransmission efficacy at the splanchnic nerve-chromaffin cell synapse of bovine adrenal medulla.

CaV1.3 as pacemaker channels in adrenal chromaffin cells: Specific role on exo- and endocytosis?

“…Bovine, rat, mouse and human adrenal chromaffin cells fire spontaneously when cultured in vitro 6,20,[30][31][32][33][34][35][36][37][38][39] or maintained in slices of the adrenal gland. 40,41 The percentage of firing chromaffin cells varies considerably (from 20 to 80%) depending review review catecholamines.…”

Blockade by Nanomolar Resveratrol of Quantal Catecholamine Release in Chromaffin Cells

“…Chromaffin cells are depolarized by ACh that produces Na ϩ -dependent action potentials that will give rise to Ca 2ϩ -dependent release of catecholamines (de Diego et al, 2008;de Diego, 2010). The possibility that resveratrol was acting on Na ϩ channels to block action potentials and secretion elicited by ACh was explored by measuring I Na in voltage-clamped cells subjected to repeated depolarizing pulses to 0 mV, given from a holding potential of Ϫ80 mV at 10-s intervals.…”

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

“…This may be due to the fact that acetylcholine elicits discrete and more localised [Ca 2+ ] c elevations, whereas K + pulses produce higher [Ca 2+ ] c transients that spread quickly throughout the cytosol [116]. This difference may be explained considering that acetylcholine evokes action potentials [117] while K + produces sustained cell depolarisation [118] in bovine chromaffin cells. Thus, it is plausible that the contribution of CICR to the exocytotic response is more visible under conditions of physiological stimulation of chromaffin cells with acetylcholine.…”

“…Direct membrane depolarisation or action potentials fired by the interaction of acetylcholine with nicotinic receptors on the surface of chromaffin cells [117] is likely the primary stimulus that induces the [Ca 2+ ] c transient, thus triggering the discharge of adrenaline and noradrenaline into the circulation [38]. Ca 2+ entry through the various subtypes of VDCCs is the primary determinant for the extent and shape of the initial [Ca 2+ ] c transient.…”