ArticleAlcoholism, clinical and experimental research2008
Role of acetaldehyde in ethanol-induced elevation of the neuroactive steroid 3alpha-hydroxy-5alpha-pregnan-20-one in rats.
Article in Alcoholism, clinical and experimental research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Inhibitors of cellular stress overcome acute effects of ethanol on hippocampal plasticity and learning.Neurobiology of disease · 2020Article
- Failure of acute ethanol administration to alter cerebrocortical and hippocampal allopregnanolone levels in C57BL/6J and DBA/2J mice.Alcoholism, clinical and experimental research · 2014Article
- Acute and chronic effects of ethanol on learning-related synaptic plasticity.Alcohol (Fayetteville, N.Y.) · 2014Review
- Locally-generated Acetaldehyde Contributes to the Effects of Ethanol on Neurosteroids and LTP in the Hippocampus.Neurology and clinical neuroscience · 2013Article
- Locally-generated acetaldehyde is involved in ethanol-mediated LTP inhibition in the hippocampus.Neuroscience letters · 2013Article
- Chronic ethanol exposure produces tolerance to elevations in neuroactive steroids: mechanisms and reversal by exogenous ACTH.Journal of neurochemistry · 2010Article
- Differential effects of ethanol on serum GABAergic 3alpha,5alpha/3alpha,5beta neuroactive steroids in mice, rats, cynomolgus monkeys, and humans.Alcoholism, clinical and experimental research · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSystemic ethanol administration increases neuroactive steroid levels that increase ethanol sensitivity. Acetaldehyde is a biologically active compound that may contribute to behavioral and rewarding effects of ethanol. We investigated the role of acetaldehyde in ethanol-induced elevations of 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP) levels in cerebral cortex.
methodsMale Sprague-Dawley rats were administered ethanol, and plasma acetaldehyde concentrations were measured by gas chromatography to determine relevant concentrations. Rats were then administered acetaldehyde directly, acetaldehyde plus cyanamide to block its degradation, or ethanol in the presence of inhibitors of ethanol metabolism, to determine effects on 3alpha,5alpha-THP levels in cerebral cortex.
resultsEthanol administration (2 g/kg) to rats results in a peak acetaldehyde concentration of 6-7 microM at 10 minutes that remains stable for the duration of the time points tested. Direct administration of acetaldehyde eliciting this plasma concentration does not increase cerebral cortical 3alpha,5alpha-THP levels, and inhibition of ethanol-metabolizing enzymes to modify acetaldehyde formation does not alter ethanol-induced 3alpha,5alpha-THP levels. However, higher doses of acetaldehyde (75 and 100 mg/kg), in the presence of cyanamide to prevent its metabolism, are capable of increasing cortical 3alpha,5alpha-THP levels.
conclusionsPhysiological concentrations of acetaldehyde are not responsible for ethanol-induced increases in 3alpha,5alpha-THP, but a synergistic role for acetaldehyde with ethanol may contribute to increases in 3alpha,5alpha-THP levels and ethanol sensitivity.
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