The adrenal medulla may mediate the increase in pineal melatonin synthesis induced by stress, but not that caused by exposure to darkness.

As previously shown (Lynch et al.: Proc. Nat.

Brain tyrosine level controls striatal dopamine synthesis in haloperidol-treated rats.

Animals received either haloperidol (2 mg/kg) or probenecid (200 mg/kg) in conjunction with tyrosine (100 mg/kg) or its diluent. Striatal homovanillic acid levels increased in probenecid-treated animals to the same range whether they were given tyrosine or not. In haloperidol-treated animals the levels of homovanillic acid were significantly elevated in animals receiving tyrosine.

Choline administration: activation of tyrosine hydroxylase in dopaminergic neurons of rat brain.

The administration of choline in doses previously shown to elevate brain acetylcholine concentrations also increases the activity of tyrosine hydroxylase in rat caudate nuclei. This response can be blocked by atropine, a muscarinic antagonist. These findings indicate that choline-induced increases in acetylcholine concentrations may be associated with parallel changes in the amount of the neurotransmitter released into synapses.

Enhancement of the anti-hypertensive effect of methyldopa and other anti-hypertensive drugs by carbidopa in spontaneously hypertensive rats.

1. A peripheral inhibitor of L-aromatic amino acid decarboxylase, carbidopa [(-)-L-alpha-hydrazino-3,4-dihydroxy-alpha-methylbenzenepropanoic acid monohydrate], at doses up to 25 mg/kg intraperitoneally or 30 mg/kg orally had no effect on directly recorded arterial pressure of spontaneously hypertensive rats derived from the Wistar/Okamoto strain. It enhanced, however, the anti-hypertensive effects of methydopa, hydrallazine, guanethidine and clonidine, and, to a lesser extent, reserpine and hydrochlorothiazide.

Melatonin in rat pineal, plasma, and urine: 24-hour rhythmicity and effect of chlorpromazine.

The concentrations of melatonin in rat pineals and in samples of rat plasma and urine were measured by bioassay or radioimmunoassay. Melatonin excretion during the daily dark period (0.98 +/- 0.

Brain acetylcholine: control by dietary choline.

Acetylcholine concentrations in whole rat brain or in various brain regions and free choline concentrations in blood serum and brain vary with dietary choline consumption. The increases in brain acetylcholine after treatment with physositigmine (an inhibitor of actylcholinesterase) or after consumption of a diet high in choline are additive, suggesting that choline acts by increasing acetylcholine synthesis.

Suppression of amphetamine-induced hypothermia by the neutral amino acid valine.

Pretreatment with valine (0.5-2.0 mmoles/kg) can suppress the hypothermic response of rats placed in a 4degreesC environment and given d-amphetamine sulfate (5 or 10 mg/kg).

The pharmacology of the pineal gland.

Only recently have a sufficient number of publications been available to legitimize a review of the pharmacology of the mammalian pineal organ. Two decades ago Kitay & Altschule reviewed the world literature on pineal physiology, which comprises several thousand papers, and concluded only that removal of the pineal, or administration of pineal extracts, somehow affected pigmentation in lower vertebrates and gonadal function in mammals (1). As the studies described below demonstrate, much more information is now available concerning the pharmacology of the pineal.

Norepinephrine turnover in the heart and spleen of the cardiomyopathic Syrian hamster.

Although a reduction in myocardial norepinephrine stores in cardiac hypertrophy and congestive failure is well documented, norepinephrine turnover has been inadequately studied in such hearts. We compared norepinephrine turnover in control and cardiomyopathic hamsters by following the decline in specific activity of myocardial norepinephrine after labelling with an intraperitoneal tracer dose of 3H-norepinephrine. Adult myocardial norepinephrine concentrations were not attained until 4 weeks of age in both strains.

Thyroid state and brain monoamine metabolism.

The rates at which rat brain synthesizes catecholamines and serotonin were estimated by measuring the accumulation of DOPA and 5-hydroxytryptophan (5-HTP) 45 min after ip administration of the decarboxylase inhibitor RO4-4602 (800 mg/kg BW). Following thyroparathy-roidectomy, hypothyroid rats showed a decreased accumulation of both precursor amino acids. On the other hand, hyperthyroidism (caused by administering 15 mug T4/100 g BW for 25 days) accelerated the accumulation of catecholamines and serotonin.

The mechanism by which methiothepin, a putative serotonin receptor antagonist, icnreses brain 5-hydroxyindole levels.

Brain tryptophan and 5-hydroxyindole levels are elevated in rats given methiothepin, a neuroleptic that appears to block serotonin receptors. The rise in brain tryptophan probably results from a drug-induced increase in the ratio of plasma tryptophan concentration to the sum of the neutral amino acids in plasma that compete with tryptophan for uptake into the brain; this change in the plasma amino acid pattern may be mediated in part by a methiothepin-induced rise in plasma insulin. Methiothepin also decreases the proportion of circulating tryptophan that is bound to albumin.