Biomedical subjects

W A Hunt

Publications and source records attributed to W A Hunt.

113 records · Page 7Linked to original sources

PubMedDate not supplied

Are binge drinkers more at risk of developing brain damage?

Alcoholism is often associated with brain damage and cognitive deficits. Because drinking patterns can include periods of alcohol consumption followed by abstinence, binge drinking may enhance the possibility of brain damage. Chronic administration of ethanol leads to upregulation of N-methyl-D-aspartate (NMDA) and calcium receptors and increased release of glucocorticoids. NMDA-mediated mechanisms and glucocorticoid actions on the hippocampus are associated with brain damage. Thus, ethanol withdrawal may make the brain more vulnerable to damage from these mechanisms, especially with binge drinking. Therapeutic adjuncts for treating ethanol withdrawal, including NMDA, calcium, and glucocorticoid antagonists, may eventually prove useful in preventing further brain damage in alcoholism.

Alcohol Drinking↗

PubMedDate not supplied

Role of acetaldehyde in the actions of ethanol on the brain--a review.

Over the last 30 years, acetaldehyde has been postulated to mediate various actions of ethanol on the brain. Experiments have studied ethanol consumption after acetaldehyde infusions into the brain, in rodents with high or low activities of hepatic and brain ethanol-metabolizing enzymes, and after treatment with drugs that alter the metabolism of acetaldehyde after ethanol ingestion. Evidence that acetaldehyde is involved in the actions of ethanol has been inconsistent because of the lack of knowledge of the brain acetaldehyde concentrations required to exert their effects, the lack of correlation between the activities of ethanol-metabolizing enzymes across strains of rodents and ethanol consumption, and the lack of specificity of drugs altering acetaldehyde metabolism. The formation of significant amounts of acetaldehyde the brain in vivo after ethanol ingestion and by what mechanism has not been clearly established, although catalase is a promising candidate. Future research needs to directly demonstrate in brain the formation of acetaldehyde in vivo, determine the concentrations in brain areas involved in ethanol consumption, and evaluate the possible actions of drugs other than an ability to block acetaldehyde metabolism.

Acetaldehyde↗

PubMedDate not supplied

Effects of subdiaphragmatic vagotomy on the acquisition of a radiation-induced conditioned taste aversion.

The effect of subdiaphragmatic vagotomy on the acquisition of a radiation-induced taste aversion was examined to assess the importance of the vagus nerve in transmitting information on the peripheral toxicity of radiation to the brain. Vagotomy had no effect on taste aversion learning, consistent with reports using other toxins. The data support the involvement of a blood-borne factor in the acquisition of taste aversion induced by ionizing radiation.

Animals↗

PubMedDate not supplied

Effects of ethanol exposure on brain sodium channels.

Ethanol, like other general anesthetics, probably acts through an interaction with excitable membranes. When ethanol is present in membranes, the lipid structure of membranes is disordered. This effect can lead to alterations in functional entities that require a particular lipid environment. Sodium channels, requiring such an environment, have been studied for their sensitivity to ethanol. In synaptosomes, ethanol in vitro reversibly inhibits sodium influx stimulated by batrachotoxin or veratridine in concentrations equivalent to those found in animals during ethanol intoxication. Only the maximum stimulation of the toxins is altered by ethanol. The potencies of aliphatic alcohols are directly related to their lipid solubilities. Acute and chronic ethanol administration reduces the effectiveness of ethanol in vitro. This tolerance dissipates after a single dose of ethanol as it is eliminated from the body. However, after 4 days of ethanol treatment, the tolerance lasts for over 20 days. These data suggest that ethanol might disrupt one of the basic processes of neural function by acting directly on the environment of the sodium channel. The channel appears to be able to adapt to the presence of ethanol through the induction of tolerance.

Animals↗

PubMedDate not supplied

Effects of area postrema lesions on taste aversions produced by treatment with WR-2721 in the rat.

The conditioned taste aversion procedure was used to further assess some behavioral effects of treatment with the putative radioprotectant WR-2721 and the role of the area postrema in mediating the behavioral effects of treatment. Treatment with 40, 150 or 300 mg/kg WR-2721 produced dose-dependent changes in sucrose intake in both control rats and rats with area postrema lesions. The effectiveness of the lesion in disrupting the acquisition of an aversion varied as a function of the dose administered, with the lesions producing the greatest disruption of aversion learning at the lowest dose and little disruption at the highest dose tested. At all dose levels, sucrose intake was greater for the rats with area postrema lesions than for the sham-operated control rats. Treatment with WR-2721 also produced significant decreases in total fluid intake, particularly at the higher dose levels. The results are discussed as indicating that treatment with WR-2721 produces highly toxic effects on behavior and that the use of the compound as a radioprotectant for radiotherapy requires additional assessment of its effects on brain function and behavior.

Amifostine↗