ArticleBritish journal of pharmacology2011
Chronic nicotine treatment differentially modifies acute nicotine and alcohol actions on GABA(A) and glutamate receptors in hippocampal brain slices.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Impacts of perinatal nicotine exposure on nicotinic acetylcholine receptor expression and glutamatergic synaptic transmission in the mouse auditory brainstem.The Journal of physiology · 2025Article
- Critical needs in drug discovery for cessation of alcohol and nicotine polysubstance abuse.Progress in neuro-psychopharmacology & biological psychiatry · 2016Review
- Snake neurotoxin α-bungarotoxin is an antagonist at native GABA(A) receptors.Neuropharmacology · 2015Article
- Neonatal nicotine exposure increases excitatory synaptic transmission and attenuates nicotine-stimulated GABA release in the adult rat hippocampus.Neuropharmacology · 2015Article
- Rare missense variants in CHRNB3 and CHRNA3 are associated with risk of alcohol and cocaine dependence.Human molecular genetics · 2014Article
- Cigarette smoke exposure greatly increases alcohol consumption in adolescent C57BL/6 mice.Alcoholism, clinical and experimental research · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
background and purposeTobacco and alcohol are often co-abused producing interactive effects in the brain. Although nicotine enhances memory while ethanol impairs it, variable cognitive changes have been reported from concomitant use. This study was designed to determine how nicotine and alcohol interact at synaptic sites to modulate neuronal processes. EXPERIMENTAL APPROACH: Acute effects of nicotine, ethanol, and both drugs on synaptic excitatory glutamatergic and inhibitory GABAergic transmission were measured using whole-cell recording in hippocampal CA1 pyramidal neurons from brain slices of mice on control or nicotine-containing diets. KEY
resultsAcute nicotine (50 nM) enhanced both GABAergic and glutamatergic synaptic transmission; potentiated GABA(A) receptor currents via activation of α7* and α4β2* nAChRs, and increased N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor currents through α7* receptors. While ethanol (80 mM) also increased GABA(A) currents, it inhibited NMDA currents. Although ethanol had no effect on AMPA currents, it blocked nicotine-induced increases in NMDA and AMPA currents. Following chronic nicotine treatment, acute nicotine or ethanol did not affect NMDA currents, while the effects of GABAergic responses were not altered. CONCLUSIONS AND IMPLICATIONS: Acute ethanol ingestion selectively attenuated nicotine enhancement of excitatory glutamatergic NMDA and AMPA receptor function, suggesting an overall reduction in excitatory output from the hippocampus. It also indicated that ethanol could decrease the beneficial effects of nicotine on memory performance. In addition, chronic nicotine treatment produced tolerance to the effects of nicotine and cross-tolerance to the effects of ethanol on glutamatergic activity, leading to a potential increase in the use of these drugs.
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