Regulation of the β-Adrenergic Receptor in the Pineal Gland and Red Cell Membranes
The pineal gland and red cell membranes have served as useful models to study the β-adrenergic receptor and its regulation. The pineal gland has a specific β-adrenergic receptor that is stimulated by noradrenaline released from nerve terminals innervating this gland. Interaction of the pineal β-adrenergic receptor triggers a series of reactions that leads to the synthesis of the pineal specific hormone melatonin. The critical biochemical step that is controlled by the β-adrenergic receptor is the synthesis of the enzyme serotonin N-acetyltransferase. The enzyme forms the precursor for the melatonin forming enzyme, hydroxyindole-0-methyltransferase. The responsiveness of the β-adrenergic receptor and the consequent synthesis of melatonin depends on the prior exposure to catecholamines. Reduced release of noradrenaline causes supersensitivity while increased exposure to catecholamine agonists results in a rapid subsensitivity. Changes in sensitivity is found not only in the β-adrenergic receptor but also in adenylate cyclase, protein kinase and other subcellular events.
KeywordsMembrane Fluidity Adrenergic Receptor Pineal Gland Pineal Cell Neurotransmitter Noradrenaline
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- Hirata, F., Viveros, O.H., Diliberto, Jr., E.J., and Axelrod, J.: Proc. Natl. Acad. Sci. USA, 1978, in press.Google Scholar