Regulation of Melatonin Release and N-Acetyltransferase Activity in Ovine Pineal Cells

A suspension culture of ovine pineal cells was developed to investigate the regulation of melatonin synthesis and release. Dosedependent stimulation of melatonin release by a series of adrenergic agonists yielded a typical β‐adrenergic profile. Serotonin N‐acetyltransferase (NAT), the rate‐limiting...

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Bibliographic Details
Published in:Journal of neuroendocrinology 1991-10, Vol.3 (5), p.477-481
Main Authors: Van Camp, Gilles, Ravault, Jean-Paul, Falcón, Jacky, Collin, Jean-Pierre, Voisin, Pierre
Format: Article
Language:English
Subjects:
adrenergic receptors
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Hormones and neuropeptides. Regulation
Hypothalamus. Hypophysis. Epiphysis. Urophysis
melatonin
N-acetyltransferase
sheep pineal
Vertebrates: endocrinology
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Summary:A suspension culture of ovine pineal cells was developed to investigate the regulation of melatonin synthesis and release. Dosedependent stimulation of melatonin release by a series of adrenergic agonists yielded a typical β‐adrenergic profile. Serotonin N‐acetyltransferase (NAT), the rate‐limiting enzyme in melatonin biosynthesis, was also stimulated by a β‐adrenergic mechanism. However, NAT activity appeared less sensitive than melatonin release to β‐adrenergic stimulation. No evidence was obtained for a contribution of α1‐adrenergic receptors to the regulation of NAT activity and melatonin release. Activation of adenylate cyclase by forskolin or addition of a cyclic AMP analogue increased both melatonin release and NAT activity. In contrast, the Ca2+ ionophore A23187 stimulated melatonin release without a detectable increase in NAT activity. Together, the present data argue for a β‐adrenergic regulation of both NAT activity and melatonin release in ovine pinealocytes. The evidence also suggests that two intracellular mechanisms may control melatonin release in ovine pinealocytes: a cyclic AMP‐dependent mechanism, associated with an increase in NAT activity and a Ca2+‐dependent mechanism, independent of NAT activity.
ISSN:0953-8194
1365-2826
DOI:10.1111/j.1365-2826.1991.tb00306.x