ArticleAddiction biology2018
Long-term subregion-specific encoding of enhanced ethanol intake by D1DR medium spiny neurons of the nucleus accumbens.
Article in Addiction biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Alcohol dependence-induced astrocyte immune activation in the nucleus accumbens.Neurobiology of disease · 2025Article
- Alcohol Dependence-Induced Astrocyte Immune Activation in the Nucleus Accumbens.bioRxiv : the preprint server for biology · 2025Article
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Striatonigral direct pathway 2-arachidonoylglycerol contributes to ethanol effects on synaptic transmission and behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Aging in nucleus accumbens and its impact on alcohol use disorders.Alcohol (Fayetteville, N.Y.) · 2023Review
- Modulation of neuronal excitability by binge alcohol drinking.Frontiers in molecular neuroscience · 2023Review
- Recent Perspectives on Sex Differences in Compulsion-Like and Binge Alcohol Drinking.International journal of molecular sciences · 2021Review
- The Sigma-2 receptor / transmembrane protein 97 (σ2R/TMEM97) modulator JVW-1034 reduces heavy alcohol drinking and associated pain states in male mice.Neuropharmacology · 2021Article
- Differential importance of nucleus accumbens Ox1Rs and AMPARs for female and male mouse binge alcohol drinking.Scientific reports · 2021Article
- Chemogenetic selective manipulation of nucleus accumbens medium spiny neurons bidirectionally controls alcohol intake in male and female rats.Scientific reports · 2020Article
- Neural Mechanisms Underlying the Rewarding and Therapeutic Effects of Ketamine as a Treatment for Alcohol Use Disorder.Frontiers in behavioral neuroscience · 2020Article
- Evidence for incentive salience sensitization as a pathway to alcohol use disorder.Neuroscience and biobehavioral reviews · 2019Review
- Modulation of Gpr39, a G-protein coupled receptor associated with alcohol use in non-human primates, curbs ethanol intake in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Ethanol Experience Enhances Glutamatergic Ventral Hippocampal Inputs to D1 Receptor-Expressing Medium Spiny Neurons in the Nucleus Accumbens Shell.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Role of glutamatergic system and mesocorticolimbic circuits in alcohol dependence.Progress in neurobiology · 2018Review
- Synaptic plasticity mechanisms common to learning and alcohol use disorder.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
- Synaptic adaptations to chronic ethanol intake in male rhesus monkey dorsal striatum depend on age of drinking onset.Neuropharmacology · 2018Article
- Chronic alcohol exposure disrupts top-down control over basal ganglia action selection to produce habits.Nature communications · 2018Article
- Cross-Species Alterations in Synaptic Dopamine Regulation After Chronic Alcohol Exposure.Handbook of experimental pharmacology · 2018Review
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The nucleus accumbens (NAc) is a critical component of the mesocorticolimbic system and is involved in mediating the motivational and reinforcing aspects of ethanol consumption. Chronic intermittent ethanol (CIE) exposure is a reliable model to induce ethanol dependence and increase volitional ethanol consumption in mice. Following a CIE-induced escalation of ethanol consumption, NMDAR (N-methyl-D-aspartate receptor)-dependent long-term depression in D1 dopamine receptor expressing medium spiny neurons of the NAc shell was markedly altered with no changes in plasticity in D1 dopamine receptor medium spiny neurons from the NAc core. This disruption of plasticity persisted for up to 2 weeks after cessation of ethanol access. To determine if changes in AMPA receptor (AMPAR) composition contribute to this ethanol-induced neuroadaptation, we monitored the rectification of AMPAR excitatory postsynaptic currents (EPSCs). We observed a marked decrease in the rectification index in the NAc shell, suggesting the presence of GluA2-lacking AMPARs. There was no change in the amplitude of spontaneous EPSCs (sEPSCs), but there was a transient increase in sEPSC frequency in the NAc shell. Using the paired pulse ratio, we detected a similar transient increase in the probability of neurotransmitter release. With no change in sEPSC amplitude, the change in the rectification index suggests that GluA2-containing AMPARs are removed and replaced with GluA2-lacking AMPARs in the NAc shell. This CIE-induced alteration in AMPAR subunit composition may contribute to the loss of NMDAR-dependent long-term depression in the NAc shell and therefore may constitute a critical neuroadaptive response underlying the escalation of ethanol intake in the CIE model.
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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.