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Biomedical subjects

W A Hunt

Publications and source records attributed to W A Hunt.

At least 91 records · Page 5Linked to original sources
PubMed1977

Alterations in brain cyclic guanosine 3':5'-monophosphate levels after acute and chronic treatment with ethanol.

A previous finding from our laboratory, that a single dose of ethanol depletes cerebellar cyclic guanosine 3':5'-monophosphate (cGMP), has now been extended to an investigation of the effects of acute and chronic ethanol treatment of cGMP levels in six areas of the rat brain. Rats were either gavaged with a single dose of ethanol (6g/kg) or rendered ethanol-dependent with 11 to 15 g/kg/day in 3 to 5 fractions over a 4-day period. A single dose of ethanol depleted cGMP levels in only five areas of the brain studied. In the two areas in which a time course of the response was determined, the caudate nucleus and cerebral cortex, cGMP depletion was maximal 1 hour after ethanol administration when blood ethanol concentrations were highest. cGMP levels returned to control values as blood ethanol was eliminated. Inethanol-dependent animals still intoxicated, cGMP was reduced but not to the same magnitude in the cerebellum and brain stem when compared with the response obtained after a single dose at equivalent blood ethanol concentrations. During the ethanol withdrawal syndrome cGMP levels had returned to control vlaues. The data suggest that cBMP depletion may play a role in ethanol-induced intoxication and that tolerance to this effect develops concurrently with behavioral tolerance.

Alcoholic Intoxication↗
PubMed1976

Suppression by 1,3-butanediol of the ethanol withdrawal syndrome in rats.

1,3-Butanediol was tested for its ability to suppress an ethanol with drawal syndrome. Male Sprague-Dawley rats were rendered physically dependent on ethanol by intragastric administration of ethanol at a dosage of 9 to 15 grams per kilogram per day over a 4-day period. A nonintoxicating oral dose of 1,3-butanediol at 4 grams per kilogram administered after elimination of ethanol from the blood was effective against the tremulous and conbulsive components of the ethanol withdrawal syndrome in all animals for 1 to 5 hours. This period coincided with the time of maximum severity of the withdrawal syndrome, as seen in the control animals.

Animals↗
PubMed1976

Temporal relationship of the induction of tolerance and physical dependence after continuous intoxication with maximum tolerable doses of ethanol in rats.

Rats were treated by intragastric intubation of a 20% ethanol solution in doses of 9-15 g/kg in 3-5 fractions for 1-7 days. Both tolerance and physical dependence were demonstrated after this treatment with the maximum tolerable doses to only a few days. Tolerance was assessed by signs of severity of intoxication: coma, loss of righting reflex, ataxia-3, ataxia-2, ataxia-1, sedation, and neutrality. During withdrawal, as blood ethanol concentrations approached 100 mg/dl the ethanol dependence phase was characterized by the onset of signs and responses of progressive severity: hyperactivity, tremors, spastic rigidity, and spontaneous convulsive seizures. A significant degree of tolerance was demonstrated for all signs of intoxication after 4 days of treatment, but did not reach maximum level even after 7 days. The severity of the withdrawal reactions intensified progressively to a maximum intensity after 4 days of treatment when as many as 72% of animals exhibited severe withdrawal signs and reactions including convulsive seizures. These different time courses suggest that tolerance and physical dependence are mediated through different mechanisms.

Alcoholism↗
PubMed1976

Ethanol-induced depletion of cerebellar guanosine 3',5' -cyclic monophosphate.

Single doses of ethanol a severe depletion (95 percent) of cerebellar guanosine 3',5' -cyclic monophosphate (cyclic GMP) within 1 hour after administration. The degree of this depletion is dose-dependent and is a function of the amount of ethanol in the blood. Interactions between ethanol and cyclic GMP may account for some of the intoxicating properties of ethanol.

Animals↗
PubMed1975

The effects of aliphatic alcohols on the biophysical and biochemical correlates of membrane function.

The simplicity of the structure of aliphatic alcohols suggests that their interaction with receptors in the classical sense is unlikely. The actions of alcohols may involve a relatively nonspecific disruption of cell membranes, possibly physically dissolving into neuronal membranes especially, resulting in the malfunction of normal physiological processes. Studies of alcohol-membrane interactions have employed the use of artificial and nonneural membranes, invertebrate neurons for electrophysiological measurements and brain tissue for studying ion fluxes and enzymatic activities. For the most part these studies have been inclusive because high concentrations of alcohols were needed to elicit any effect. Also, it is difficult to extrapolate the data to in vivo mammalian systems, especially relative to the clinical signs of depression of the central nervous system.

Action Potentials↗