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Prostaglandins Stimulate Serotonin Acetylation in Chick Pineal Cells: Involvement of Cyclic AMP‐Dependent and Calcium/Calmodulin‐Dependent Mechanisms
Author(s) -
Voisin P.,
Camp G.,
Pontoire C.,
Collin J. P.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03199.x
Subject(s) - serotonin , calmodulin , calcium , endocrinology , medicine , pineal gland , chemistry , acetylation , microbiology and biotechnology , biology , biochemistry , melatonin , receptor , gene
The effects of prostaglandins (PGs) on the activity of the rate‐limiting enzyme of melatonin biosynthesis, aryl‐alkylamine‐ N ‐acetyltransferase (NAT) were investigated on primary cultures of dispersed chick pineal cells. In indomethacin‐treated cells, PGs caused a four‐fold increase in NAT activity. This response was associated with an eightfold increase in cyclic AMP (cAMP) levels. The potency order of PGs was the same for NAT and for cAMP responses (PGE 1 > PGE 2 > PGF 2α ≫ cloprostenol). However, each PG tested was 30‐ to 200‐fold more potent to increase NAT activity than to stimulate cAMP accumulation. As a result, half‐maximal stimulation of NAT by PGs was not associated with an increase in cAMP levels. Half‐maximal stimulation of NAT by PGE 1 was highly sensitive to inhibition by a calcium/calmodulin antagonist (W‐7). In contrast, maximal stimulation of NAT by PGE 1 as well as stimulations evoked by either forskolin or 8‐bromo‐cAMP were poorly sensitive to inhibition by W‐7. These results indicate that an increase in cAMP levels may be responsible for the maximal stimulation of NAT evoked by PGs, whereas half‐maximal stimulation of NAT by PGs would rely principally on a calcium/calmodulin‐dependent mechanism.