Gap junction signalling is a stress-regulated component of adrenal neuroendocrine stimulus-secretion coupling in vivo

Michel G. Desarménien, Carole Jourdan, Bertrand Toutain, Emilie Vessières, Sheriar G. Hormuzdi and Nathalie C. Guérineau ()
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Michel G. Desarménien: CNRS, UMR-5203, Institut de Génomique Fonctionnelle
Carole Jourdan: CNRS, UMR-5203, Institut de Génomique Fonctionnelle
Bertrand Toutain: Department of Integrated Neurovascular and Mitochondrial Biology
Emilie Vessières: Department of Integrated Neurovascular and Mitochondrial Biology
Sheriar G. Hormuzdi: Ninewells Hospital and Medical School, University of Dundee
Nathalie C. Guérineau: Department of Integrated Neurovascular and Mitochondrial Biology

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: Abstract Elucidating the mechanisms whereby neuroendocrine tissues coordinate their input and output signals to ensure appropriate hormone secretion is currently a topical issue. In particular, whether a direct communication mediated by gap junctions between neurosecretory cells contributes to hormone release in vivo still remains unknown. Here we address this issue using a microsurgical approach allowing combined monitoring of adrenal catecholamine secretion and splanchnic nerve stimulation in anaesthetised mice. Pharmacological blockade of adrenal gap junctions by the uncoupling agent carbenoxolone reduces nerve stimulation-evoked catecholamine release in control mice and to a larger extent in stressed mice. In parallel, the gap junction-coupled cell network is extended in stressed mice. Altogether, this argues for a significant contribution of adrenomedullary gap junctions to catecholamine secretion in vivo. As such, gap junctional signalling appears to be a substantial component for neuroendocrine function in the adrenal medulla, as it may represent an additional lever regulating hormone release.

Date: 2013
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DOI: 10.1038/ncomms3938

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