Glutamate Inhibition of the Adrenergic‐Stimulated Production of Melatonin in Rat Pineal Gland In Vitro

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Abstract
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 (beta-adrenergic agonist) and L-phenylephrine (alpha-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.