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Glutamate Inhibition of the Adrenergic‐Stimulated Production of Melatonin in Rat Pineal Gland In Vitro
Author(s) -
Kus Laura,
Handa Robert J.,
McNulty John A.
Publication year - 1994
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 - 10.1046/j.1471-4159.1994.62062241.x
Subject(s) - melatonin , glutamate receptor , kainate receptor , phenylephrine , agonist , medicine , endocrinology , pineal gland , adrenergic , biology , chemistry , receptor , ampa receptor , blood pressure
The effect of l ‐glutamate on the adrenergic‐stimulated release of melatonin in the rat pineal gland was examined using an in vitro perfusion system. l ‐Glutamate by itself had no effect on melatonin secretion whereas l ‐glutamate administered prior to (–)‐isoproterenol (β‐adrenergic agonist) and l ‐phenylephrine (α‐adrenergic agonist) inhibited melatonin production by 42%. l ‐Glutamate did not inhibit melatonin secretion when glands were stimulated with (–)‐isoproterenol alone. d ‐Glutamate, as well as the l ‐glutamate agonists kainate, N ‐methyl‐ d ‐aspartate, quisqualate, and trans ‐1‐aminocyclopentane‐1, 3‐dicarboxylic acid, had no effect on the (–)‐isoproterenol‐and l ‐phenylephrine‐stimulated secretion of melatonin, which suggests that the inhibitory effects of glutamate are not mediated via any of the known glutamate receptor subtypes. The possibility that l ‐glutamate may be converted to another neuroactive compound (GABA) prior to the addition of (–)‐isoproterenol and l ‐phenylephrine is suggested by the observation that simultaneous administration of l ‐glutamate with (–)‐isoproterenol and l ‐phenylephrine did not inhibit melatonin production.