Search PubMed⌕ Search

Biomedical subjects

B Tabakoff

Publications and source records attributed to B Tabakoff.

At least 199 records · Page 11Linked to original sources
PubMed1979

Development of functional dependence on ethanol in dopaminergic systems.

Withdrawal of mice from chronic ethanol treatment results in a decreased responsiveness of striatal (but not mesolimbic) dopamine-sensitive adenylate cyclase activity to stimulation by dopamine. This subsensitivity is not apparent at the time of withdrawal from chronic feeding of ethanol, when animals are still intoxicated, but becomes evident as ethanol is eliminated from the animals. Addition of ethanol in vitro to tissue homogenates from ethanol-withdrawn animals, at concentrations similar to those found in brain at the time of withdrawal, normalizes the response of the adenylate cyclase to dopamine. No difference is evident between control and ethanol-withdrawn animals in stimulation of adenylate cyclase by sodium fluoride. The specificity of the response of striatal adenylate cyclase to stimulation by dopamine, as compared to other transmitters, is unaltered by chronic ethanol feeding. Chronic treatment with ethanol and withdrawal also does not affect the specific binding of spiroperidol in either striatal or mesolimbic regions. It is suggested that the decreased response of adenylate cyclase to dopamine in ethanol-withdrawn animals results from decreased efficiency of coupling between dopamine "receptor" sites and catalytic units of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1978

Brain noradrenergic systems as a prerequisite for developing tolerance to barbiturates.

Mice treated with 6-hydroxydopamine before they were chronically fed phenobarbital did not develop functional barbiturate tolerance, measured by duration of the loss of righting reflex and hypothermia. Injection of 6-hydroxydopamine caused significant depletion of brain norepinephrine, while brain dopamine levels were not significantly depleted. Intact brain noradrenergic systems seem to be necessary for developing tolerance to the hypnotic and hypothermic effects of the barbiturates.

Animals↗
PubMed1978

Corticosterone concentrations in mice during ethanol drinking and withdrawal.

Consumption of an ethanol-containing diet by mice resulted in a significant increase in circulating concentrations of corticosterone which was maintained for 8 days. There were no changes in the concentrations of plasma corticosterone binding globulin. Ethanol withdrawal symptoms followed the removal of ethanol from the diet and circulating corticosterone concentrations were further increased. There was no correlation between blood ethanol and glucocorticoid concentrations during the chronic ethanol treatment. Stress related to ethanol consumption may be of greater importance than the circulating ethanol concentrations in producing the elevation in plasma glucocorticoids.

Alcoholism↗
PubMed1977

Effects of tranylcypromine and pargyline on brain tryptamine.

Tranylcypromine produces behavioral excitation while pargyline produces depression. Tranylcypromine increased brain tryptophan which led to an accumulation of tryptamine. The levels of tryptamine after tranylcypromine were found to be 3 times those found after pargyline.

Animals↗
PubMed1977

Role of catecholamines in the development of tolerance to barbiturates and ethanol.

The destruction of noradrenergic systems in brain by administration of 6-hydroxydopamine prior to chronic ethanol treatment prevented the development of tolerance to ethanol. Animals pretreated with 6-hydroxy dopamine also showed no cross tolerance to barbiturates. Destruction of noradrenergic systems prior to chronic treatment with barbiturates also partially prevented the development of tolerance to pentobarbital. 6-Hydroxydopamine pretreatment had little effect on the signs of physical dependence produced by ethanol. The possible dissociation of tolerance and dependence and the role of noradrenergic systems in these phenomena is discussed.

Animals↗
PubMed1977

Neurochemical correlates of ethanol withdrawal: alterations in serotoninergic function.

Cessation of chronic ethanol administration, and elimination of ethanol from the body, results in a withdrawal syndrome in mice characterized by behavioural symptoms and hypothermia. During withdrawal, the accumulation rate of [14C] 5-hydroxytryptamine (5-HT) from [14C]tryptophan, was significantly lower in the brainstem of the ethanol-withdrawn animals than in controls. A similar pattern was seen in forebrain. When the rate of 5-HT accumulation was determined using pargyline, no differences occurred between control and ethanol-treated animals. The endogenous concentrations of tryptophan in plasma, and tryptophan, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in brain were the same in ethanol-treated and control animals. It is suggested that the changes in accumulation of 14C-5-HT and 14C-5-HIAA in ethanol-withdrawn animals reflected alterations in electrical activity of serotoninergic neurons during withdrawal.

Alcoholism↗
PubMed1977

The effects of 6-hydroxydopamine on tolerance to and dependence on ethanol.

The intraventricular administration of 6-hydroxydopamine before chronic ethanol exposure prevented the development of tolerance to the hypnotic and hypothermic effects of ethanol as well as cross-tolerance to barbiturates. The injection of 6-hydroxydopamine depleted brain norepinephrine but had little effect on levels of dopamine and serotonin. Although mice pretreated with 6-hydroxydopamine did not develop tolerance to ethanol, they exhibited signs of physical dependence after chronic treatment with ethanol. If 6-hydroxydopamine was administered after tolerance to ethanol was established, the destruction of noradrenergic neurons had little effect in disrupting the tolerance. Noradrenergic systems may be necessary for the "consolidation" but not the expression of tolerance.

Alcoholism↗