NDLI: Vasoactive Intestinal Peptide Stimulates Chick Pineal Melatonin Production and Interacts with Other Stimulatory and Inhibitory Agents but Does Not Show ?1-Adrenergic Potentiation

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Vasoactive Intestinal Peptide Stimulates Chick Pineal Melatonin Production and Interacts with Other Stimulatory and Inhibitory Agents but Does Not Show ?1-Adrenergic Potentiation

Content Provider	Scilit
Author	Zatz, Martin Kasper, Gabriel Marquez, Christopher R.
Copyright Year	1990
Description	Journal: Journal of Neurochemistry Vasoactive intestinal peptide (VIP) is known to mimic the effects of beta-adrenergic receptor stimulation in the rat pineal, including marked potentiation by alpha 1-adrenergic receptor stimulation, and to cause increased melatonin synthesis. In contrast, the chick pineal does not respond to beta-adrenergic stimulation, and melatonin synthesis is inhibited by norepinephrine via an alpha 2-adrenergic receptor. The present experiments show that chick pineal cells in primary culture do, however, respond to VIP with increased melatonin production. The effect of VIP was inhibited by addition of norepinephrine or of nitrendipine or by exposing the cells to "unexpected" white light. Stimulation by VIP was enhanced by addition of forskolin or Bay K 8644 but not by alpha 1-adrenergic receptor stimulations. Although stimulation by VIP appears similar in the chick pineal to that seen in the rat pineal and other systems, "dual-receptor regulation," at least with alpha 1-adrenergic receptors, appears to be absent.
Related Links	http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.1990.tb03118.x/pdf
Ending Page	1153
Page Count	5
Starting Page	1149
e-ISSN	14714159
DOI	10.1111/j.1471-4159.1990.tb03118.x
Journal	Journal of Neurochemistry
Issue Number	4
Volume Number	55
Language	English
Publisher	Wiley-Blackwell
Publisher Date	1990-10-01
Access Restriction	Open
Subject Keyword	Journal: Journal of Neurochemistry Endocrinology and Metabolism Vasoactive Intestinal Peptide Melatonin Production Α1‐adrenergic Receptors
Content Type	Text
Resource Type	Article

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