Yoshinori Moriyama, Hiroshi Yamada, Mitsuko Hayashi, and Shouki Yatsushiro

Department of Cell Membrane Biology

Institute of Scientific and Industrial Research (ISIR)

Osaka University

Ibaraki Osaka 567-0047, Japan

The mammalian pineal gland is a photoneuroendocrine transducer that rhythmically synthesizes and secretes melatonin at night in response to photoperioic stimuli and signals from endogenous circadian oscillators (1-3). In the rat, this process is controlled by the suprachiasmatic nuclei (SCN) through sympathetic neurons projecting into the glands. These neurons secrete norepinephrine (NE) which binds to adrenergic receptors and activates adenylate cyclase through a heterotrimeric guanine nucleotide -binding protein (Gs). The resultant increase of cAMP causes transcriptional activation of the serotonin N-acetyltransferase (NAT), resulting in increased melatonin output (4). Thus, the role of sympathetic innervation as a positive regulatory mechanism for melatonin synthesis has been firmly established. However, the daily change of NAT mRNA and its activity are not completely correlated with the rate of decrease of NAT activity, suggesting the presence of regulatory mechanism(s) other than adrenergic one in pineal gland.

From the studies on the structure and function of synaptic-like microvesicles (or microvesicle; MVs) in bovine pineal gland (5-7), we have learned that pinealo-cytes are glutaminergic neuroendocrine cells, and use L-glutamate as a negative regulator for melatonin synthesis (Figure 1). In this article, we describe briefly the mechanism by which the glutaminergic system inhibits melatonin synthesis in pineal gland.

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Mammalian pinealocytes use EAAs as negative regulators for melatonin synthesis. Mammalian Pinealocytes Are Glutaminergic Endocrine Cells^)

Figure 1. Glutaminergic systems in rat pineal gland.

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