Search PubMed⌕ Search

Biomedical subjects

J L Weller

Publications and source records attributed to J L Weller.

At least 55 records · Page 3Linked to original sources
PubMed1980

Evidence of inactivation of pineal indoleamine N-acetyltransferase by protein thiol:disulfide exchange.

Pineal indoleamine N-acetyltransferase activity in homogenates is rapidly reduced at pH 6.8 by treatment with cystamine or arginine vasotocin. Other disulfides including glutathione disulfide, penicillamine disulfide, and N,N'-diacetylcystamine are either ineffective or less effective. The diamine analogous to cystamine, diaminohexane, is also ineffective. Inactivation by cystamine is accelerated at higher pH and is temperature- and time-dependent. It was also found that cystamine treatment inactivated N-acetyltransferase in intact pineal cells. Treatment with dithiothreitol reactivated the cystamine- or arginine vasotocin-inactivated enzyme formed in broken cell preparations and the cystamine-inactivated enzyme formed in intact cells. These observations indicate that pineal N-acetyltransferase can be inactivated by protein thiol:disulfide exchange; further research is required to ascertain whether this mechanism is of physiological significance.

Acetyltransferases↗
PubMed1979

Taurine: stimulation of pineal N-acetyltransferase activity and melatonin production via a beta-adrenergic mechanism.

Pineal glands convert [3H]tryptophan to [3H]N-acetylserotonin and [3H]melatonin in organ culture. Taurine treatment increases the rate of production of these compounds 40- and 25-fold respectively by stimulating the activity of N-acetyltransferase. This stimulation is blocked stereospecifically by L-propranolol, indicating that taurine is probably acting via beta-adrenergic receptors. Taurine is active in stimulating N-acetyltransferase activity in denervated glands, suggesting that it might interact directly with the beta-adrenergic receptor, and not by causing the release of norepinephrine from nerve terminals.

Acetylserotonin O-Methyltransferase↗
PubMed1977

Adrenergic control of pineal N-acetyltransferase activity: developmental aspects.

The activity of pineal N-acetyltransferase in the neonatal rat does not exhibit the large daily rhythm seen in the adult and is intermediate between the low day and high night adult values. These intermediate values appear to result from adrenergic stimulation. Blockade of adrenergic receptors or of catecholamine synthesis results in a decrease in enzyme activity in vivo. In vitro studies provide additional evidence of a completely developed postsynaptic adrenergic control system for pineal N-acetyltransferase activity at birth. Our observations indicate that the appearance of a circadian rhythm in pineal N-acetyltransferase at the end of the first week of life reflects the development of presynaptic mechanisms and structures necessary for the control of catecholamine release and uptake. These events follow the developmental appearance of the postsynaptic mechanisms required to mediate the adrenergic-cycle AMP regulation of pineal N-acetyltransferase activity, which can be detected prior to birth.

Acetyltransferases↗
PubMed1976

On GABA function and physiology in the pineal gland.

Pineal gamma-aminobutyric acid (GABA) content and glutamic acid decarboxylase (GAD) activity were found not to be influenced by environmental light, catecholamines, sympathetic innervation, or input via the pineal stalk. The observation that GAD activity did not disappear after pineal stalk section, ganglionectomy, or 48 h of organ culture leads us to suggest that GAD activity is not located in nerve processes entering the pineal gland. Treatment in organ culture with an inhibitor of protein synthesis did not greatly influence the slow rate of decrease of GAD activity. This finding is consistent with the conclusion that GAD turnover is slow. Treatment of denervated glands or glands containing functional sympathetic nerve structures with GABA, amino-oxyacetic acid (AOAA) or bicuculline in organ culture did not alter unstimulated levels, or significantly block the adrenergic stimulation of the activity of pineal serotonin N-acetyl transferase (NAT). It is clear from our studies that GABA does not influence or modulate the adrenergic regulation of.pineal NAT activity, and that GABA content and synthesis are not regulated by an adrenergic mechanism. The role of GABA in the pineal gland remains to be discovered.

Acetylcholinesterase↗
PubMed1972

Rapid light-induced decrease in pineal serotonin N-acetyltransferase activity.

Light acting by way of the eye causes the dark-induced activity of serotonin N-acetyltransferase in the pineal gland of the rat to decrease with a halving time of about 3 minutes. This effect, which is one of the more rapid physiological changes known to occur in the activity of any enzyme that metabolizes biogenic amines, appears to explain the rapid increase in the concentration of pineal serotonin that is caused by light exposure at night.

Acyltransferases↗
PubMed1971

Melatonin metabolism: neural regulation of pineal serotonin: acetyl coenzyme A N-acetyltransferase activity.

There is a diurnal rhythm in the activity of serotonin N-acetyltransferase in the rat pineal gland. In the normal rat, the nocturnal enzyme activities are 15-to 30-fold greater than are daytime activities. This rhythm is abolished by decentralization or removal of the superior cervical ganglia, procedures that interrupt the only source of central neural input to the pineal gland. This effect of superior cervical sympathectomy on the N-acetyltransferase rhythm cannot be attributed to changes occurring in the denervated pineal parenchymal cells. When chronically denervated glands are placed in organ culture with norepinephrine, the neurotransmitter normally located in sympathetic terminals in the gland, N-acetyltransferase activity increases 10- to 20-fold. These data indicate that superior cervical sympathectomy abolishes the N-acetyltransferase rhythm by elimination of the input of central signals to the gland. These signals appear to regulate the N-acetyltransferase rhythm in the normal rat by regulation of the release of norepinephrine from the sympathetic terminals within the pineal gland.

Acyltransferases↗