Interaction between pargyline, a monoamine oxidase inhibitor, and beta-adrenergic receptors in the rat pineal gland.

The hypothesis that pargyline, a monoamine oxidase inhibitor, may interact with pineal beta-adrenergic receptors to increase N-acetyltransferase (NAT) activity and, thereby, melatonin content was tested in intact and superior cervical ganglionectomized (SCGX) rats some of which were also treated with the tryptophan hydroxylase inhibitor para-chlorophenylalanine (PCPA). Pargyline injection increased both NAT activity and melatonin content, an effect nullified by conjunct propranolol injection. While pargyline injection also increased NAT activity in intact, PCPA-treated rats, the effects of this drug were most evident in SCGX, PCPA-treated rats. PCPA treatment prevented pargyline-induced increases in melatonin content in intact and SCGX rats suggesting an artificially-induced dissociation of melatonin biosynthesis from its rate-limiting enzyme. We suggest that pargyline may be capable of interacting with pineal beta-adrenergic receptors to increase NAT activity in the absence of pineal norepinephrine (NE) and serotonin.