ArticleNeuropharmacology2023
Alcohol potentiates multiple GABAergic inputs to dorsal striatum fast-spiking interneurons.
Article in Neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Anterior cingulate cortex activation of claustrum projection neuron subtypes is enhanced by alcohol.Neuropharmacology · 2026Article
- Perineuronal Net and Inhibitory Synapse Remodeling on Striatal Fast-Spiking Interneurons by Chronic Alcohol Exposure.Biological psychiatry · 2026Article
- Alcohol Withdrawal Alters the Inhibitory Landscape of the Prelimbic Cortex in an Interneuron- and Sex-specific Manner.Addiction neuroscience · 2025Article
- A single-cell genomic atlas for the effects of chronic ethanol exposure in the mouse dorsal striatum.Molecular psychiatry · 2025Article
- Alcohol effects on associative and sensorimotor cortico-thalamo-basal ganglia circuits alter decision making and alcohol intake.Alcohol (Fayetteville, N.Y.) · 2025Review
- Associative memory in alcohol-related contexts: An fMRI study with young binge drinkers.Journal of psychopharmacology (Oxford, England) · 2024Article
- A paradigm for ethanol consumption in head-fixed mice during prefrontal cortical two-photon calcium imaging.Neuropharmacology · 2024Article
- Chronic alcohol exposure differentially alters calcium activity of striatal cell populations during actions.Addiction neuroscience · 2023Article
- A paradigm for ethanol consumption in head-fixed mice during prefrontal cortical two-photon calcium imaging.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Parvalbumin-expressing dorsal striatal fast-spiking interneurons, comprising ∼1% of the total dorsal striatal neuronal population, are necessary for the expression of compulsive-like ethanol consumption mice. Fast-spiking interneurons are driven to fire by glutamatergic inputs derived primarily from the cortex. However, these neurons also receive substantial GABAergic input from two sources: the globus pallidus and the reticular nucleus of the thalamus. How ethanol modulates inhibitory input onto fast-spiking neurons is unclear and, more broadly, alcohol effects on GABAergic synaptic transmission onto GABAergic interneurons are understudied. Examining this, we found that acute bath application of ethanol (50 mM) potentiated GABAergic transmission from both the globus pallidus and the reticular nucleus of the thalamus onto fast-spiking interneurons in mouse of both sexes. This ethanol-induced potentiation required postsynaptic calcium and was not accompanied by a sustained change in presynaptic GABA release probability. Examining whether this ethanol effect persisted following chronic intermittent ethanol exposure, we found attenuated acute-ethanol potentiation of GABAergic transmission from both the globus pallidus and the reticular nucleus of the thalamus onto striatal fast-spiking interneurons. These data underscore the impact of ethanol on GABAergic signaling in the dorsal striatum and support the notion that ethanol may disinhibit the dorsolateral striatum.
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