ArticleSynapse (New York, N.Y.)2010
Decreased Beta(2)*-nicotinic acetylcholine receptor availability after chronic ethanol exposure in nonhuman primates.
Article in Synapse (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Cognitive-Enhancing Effects of Acetylcholine Receptor Agonists in Group-Housed Cynomolgus Monkeys Who Drink Ethanol.The Journal of pharmacology and experimental therapeutics · 2024Article
- Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum.Alcoholism, clinical and experimental research · 2021Article
- The Impact of Adolescent Alcohol Exposure on Nicotine Behavioral Sensitization in the Adult Male Neonatal Ventral Hippocampal Lesion Rat.Frontiers in behavioral neuroscience · 2021Article
- Adolescent alcohol exposure decreased sensitivity to nicotine in adult Wistar rats.Addiction biology · 2016Article
- How Imaging Glutamate, γ-Aminobutyric Acid, and Dopamine Can Inform the Clinical Treatment of Alcohol Dependence and Withdrawal.Alcoholism, clinical and experimental research · 2015Review
- Changes in the α4β2* nicotinic acetylcholine system during chronic controlled alcohol exposure in nonhuman primates.Drug and alcohol dependence · 2014Article
- Recent advances in understanding nicotinic receptor signaling mechanisms that regulate drug self-administration behavior.Biochemical pharmacology · 2011Review
- Neuroimaging insights into the role of cortical GABA systems and the influence of nicotine on the recovery from alcohol dependence.Neuropharmacology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Ethanol associated behaviors have been linked to the beta(2)-subunit containing nicotinic acetylcholine receptors (beta(2)*-nAChR); however, there is conflicting evidence on ethanol-induced changes in nAChR expression during and after chronic ethanol consumption. In this study, five male animals orally self-administered ethanol for 18 +/- 1 weeks. Animals were scanned with [(123)I]5-IA-85380 and SPECT prior to ethanol self-administration, and at 24 h and 5-13 wks withdrawal. beta(2)*-nAChR availability was not significantly different from baseline at 24 h withdrawal, but was significantly decreased compared to baseline at 5-13 wks withdrawal throughout the cortex and in the thalamus, but not the midbrain. The percent decrease in beta(2)*-nAChR availability from baseline to 5-13 wks withdrawal in the parietal cortex was negatively correlated with total grams of ethanol consumed in lifetime and in the midbrain was negatively correlated with average daily ethanol consumption (g/kg). Prolonged withdrawal from chronic ethanol consumption is associated with a decrease in beta(2)*-nAChR availability. The decrease in beta(2)*-nAChR availability is influenced by alcohol consumption, suggesting the chronicity and severity of alcohol consumption may underlie persistent changes in beta(2)*-nAChR availability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.