Metabotropic Glutamate Receptors Negatively Regulate Melatonin Synthesis in Rat Pinealocytes

Rat pinealocytes receive noradrenergic innervation that stimulates melatonin synthesis in a cAMP-mediated manner. In addition to melatonin, we showed previously that pinealocytes secrete L-glutamate through an exocytic mechanism. The released glutamate inhibits norepinephrine (NE)-dependent melatoni...

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Bibliographic Details
Published in:The Journal of neuroscience 1998-03, Vol.18 (6), p.2056-2062
Main Authors: Yamada, Hiroshi, Yatsushiro, Shouki, Ishio, Shougo, Hayashi, Mitsuko, Nishi, Tsuyoshi, Yamamoto, Akitsugu, Futai, Masamitsu, Yamaguchi, Akihito, Moriyama, Yoshinori
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Glutamic Acid - pharmacology
GTP-Binding Proteins - metabolism
Melatonin - antagonists & inhibitors
Melatonin - biosynthesis
Norepinephrine - pharmacology
Pineal Gland - cytology
Pineal Gland - metabolism
Rats
Rats, Wistar
Receptors, Metabotropic Glutamate - agonists
Receptors, Metabotropic Glutamate - physiology
Tissue Distribution
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Summary:Rat pinealocytes receive noradrenergic innervation that stimulates melatonin synthesis in a cAMP-mediated manner. In addition to melatonin, we showed previously that pinealocytes secrete L-glutamate through an exocytic mechanism. The released glutamate inhibits norepinephrine (NE)-dependent melatonin synthesis. Consistent with this observation, specific agonists of class II metabotropic glutamate receptors (mGluRs), including 1-(1S,3R)-aminocyclopentane-1,3-dicarboxylic acid (tACPD), inhibited NE-dependent melatonin synthesis, whereas agonists for other types of glutamate receptors did not. Furthermore, reverse transcription-PCR, Northern blotting, and immunohistochemistry analyses indicated expression of class II mGluR3 in pinealocytes. Inhibitory guanine nucleotide-binding protein (Gi) was also detected in pinealocytes. L-Glutamate or agonists of class II receptors decreased NE- or forskolin-dependent increase of cAMP and serotonin-N-acetyltransferase activities to similar extents. These effects were blocked by pertussis toxin or dibutyryl cAMP. These results indicate that the inhibitory cAMP cascade is involved in the glutamate-evoked inhibition of melatonin synthesis. We propose that the glutaminergic system negatively regulates NE-dependent melatonin synthesis in rat pinealocytes.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.18-06-02056.1998