Functional synaptogenesis and the rat pineal gland: a pharmacological investigation

Pineal glands obtained from rats of different ages were incubated in vitro with drugs known to specifically alter pre- or postsynaptic noradrenergic neurotransmission to determine when during development nerve terminal or receptor mediated control of glandular N-acetyltransferase (NAT) activity might reach functional maturation. Basal daytime NAT activity measured in vitro was lowest in fetal rats, increased dramatically by the day of birth, peaked at 10 days postnatally, and subsequently declined to near adult levels by 25 days of age. Drugs (isoproterenol, norepinephrine, or propranolol) known to influence pineal gland NAT activity by acting directly on pinealocyte postsynaptic beta-noradrenoceptors produced comparable changes in enzyme activity at all ages studied, although larger doses of the receptor agonist were required in fetal animals to elevate NAT activity. In contrast, in vitro incubation with indirect acting drugs (amphetamine or 1-dopa) which require functional presynaptic nerve terminals to exert their pharmacological effects, failed to increase pineal gland NAT activity until early in postnatal life. Hence, postsynaptic beta-noradrenoceptors may function to control pineal gland NAT activity prior to the time when the presynaptic sympathetic neurons innervating the gland attain maturational status.