Integrated Mitochondrial and Neurovascular Biology, CNRS UMR6214, INSERM U1083, University of Angers, UFR Sciences Médicales, 1 rue Haute de Reculée, 49045 Angers CEDEX 01, France.
J Mol Neurosci. 2012 Oct;48(2):368-86. doi: 10.1007/s12031-012-9707-7. Epub 2012 Jan 18.
An increase in circulating catecholamines constitutes one of the mechanisms whereby human body responds to stress. In response to chronic stressful situations, the adrenal medullary tissue exhibits crucial morphological and functional changes that are consistent with an improvement of chromaffin cell stimulus-secretion coupling efficiency. Stimulus-secretion coupling encompasses multiple intracellular (chromaffin cell excitability, Ca(2+) signaling, exocytosis, endocytosis) and intercellular pathways (splanchnic nerve-mediated synaptic transmission, paracrine and endocrine communication, gap junctional coupling), each of them being potentially subjected to functional remodeling upon stress. This review focuses on three chromaffin cell incontrovertible actors, the cholinergic nicotinic receptors and the voltage-dependent T-type Ca(2+) channels that are directly involved in Ca(2+)-dependent events controlling catecholamine secretion and electrical activity, and the gap junctional communication involved in the modulation of catecholamine secretion. We show here that these three actors react differently to various stressors, sometimes independently, sometimes in concert or in opposition.
循环儿茶酚胺的增加构成了人体应对压力的机制之一。在应对慢性应激情况时，肾上腺髓质组织表现出与嗜铬细胞刺激-分泌偶联效率提高相一致的关键形态和功能变化。刺激-分泌偶联包含多个细胞内（嗜铬细胞兴奋性、Ca(2+)信号、胞吐、胞吞）和细胞间途径（内脏神经介导的突触传递、旁分泌和内分泌通讯、缝隙连接偶联），其中每一种途径都可能在受到应激时发生功能重塑。这篇综述重点介绍了三个不可否认的嗜铬细胞作用因子，即胆碱能烟碱受体和电压依赖性 T 型 Ca(2+)通道，它们直接参与控制儿茶酚胺分泌和电活动的 Ca(2+)-依赖性事件，以及参与调节儿茶酚胺分泌的缝隙连接通讯。我们在这里表明，这三个作用因子对各种应激源的反应不同，有时是独立的，有时是协同的，有时是相反的。
