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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/C407    most recent 00086.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Fernández-Morales, J. C. Articles by de Diego, A. M. G. PubMed PubMed Citation Articles by Fernández-Morales, J. C. Articles by de Diego, A. M. G.

NERVOUS SYSTEM CELL BIOLOGY

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

¹Instituto Teófilo Hernando, ²Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, and ³Servicio de Farmacología Clínica, Hospital Universitario de la Princesa and Universidad Autónoma de Madrid, Madrid, Spain

Submitted 25 February 2009 ; accepted in final form 10 May 2009

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 Ca²⁺ entry by L-type Ca²⁺ channel activator BAY K 8644 did not change the kinetic parameters of single spikes in ECCs; in contrast, augmentation of Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ channel blockers may augment the incidence of sudden infant death syndrome (SIDS); and 3) so-called Ca²⁺ promotors or activators of Ca²⁺ 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.

rat chromaffin cell; quantal catecholamine secretion; exocytosis; amperometry; calcium channels