NDLI: Differences in the quantal release of catecholamines in chromaffin cells of rat embryos and their mothers.

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Differences in the quantal release of catecholamines in chromaffin cells of rat embryos and their mothers.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fernández-Morales, José C. Cortés-Gil, Lorena García, Antonio G. de Diego, Antonio M. G.
Description	Country affiliation: Spain Author Affiliation: Fernández-Morales JC ( Instituto Teófilo Hernando, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.)
Abstract	Studies on the bulk catecholamine release from fetal and neonatal rat adrenals, adrenal slices, or isolated chromaffin cells stimulated with high K(+), hypoxia, hypercapnia, or acidosis are available. However, a study analyzing the kinetics of quantal secretion is lacking. We report here such a study in which we compare the quantal release of catecholamines from immature rat embryo chromaffin cells (ECCs) and their mothers' (MCCs). Cell challenging with a strong depolarizing stimulus (75 mM K(+)) caused spike bursts having the following characteristics. ECCs released more multispike events and wave envelopes than MCCs. This, together with narrower single-spike events, a faster decay, and a threefold smaller quantal size suggest a faster secretory machinery in ECCs. Furthermore, with a milder stimulus (25 mM K(+)) enhanced Ca(2+) entry by L-type Ca(2+) channel activator BAY K 8644 did not change the kinetic parameters of single spikes in ECCs; in contrast, augmentation of Ca(2+) entry increased spike amplitude and width, quantal size, and decay time in MCCs. This suggests that in mature MCCs, the last exocytotic steps are more tightly regulated than in immature ECCs. Finally, we found that quantal secretion was fully controlled by L-type voltage-dependent Ca(2+) channels (VDCCs) in ECCs, whereas both L- and non-L VDCCs (N and PQ) contributed equally to secretion control in MCCs. Our results have the following physiological, pharmacological, and clinical relevance: 1) they may help to better understand the regulation of adrenal catecholamine release in response to stress during fetal life and delivery; 2) if clinically used, L-type Ca(2+) channel blockers may augment the incidence of sudden infant death syndrome (SIDS); and 3) so-called Ca(2+) promotors or activators of Ca(2+) entry through L-type VDCCs may be useful to secure a healthy catecholamine surge upon violent stress during fetal life, at birth, or to prevent the SIDS in neonates at risk.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	2
Volume Number	297
Language	English
Publisher	American Physiological Society
Publisher Date	2009-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Catecholamines Secretion Chromaffin Cells Embryo, Mammalian Metabolism Adrenal Medulla Cytology Animals Calcium Channel Agonists Calcium Channel Blockers Calcium Channels Nimodipine Potassium Pregnancy Rats, Wistar Omega-conotoxins Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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