ArticleJournal of neurophysiology2014
Plasticity of GABA(A) receptor-mediated neurotransmission in the nucleus accumbens of alcohol-dependent rats.
Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- 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
- Changes in neuronal excitability and synaptic transmission in nucleus accumbens in a transgenic Alzheimer's disease mouse model.Scientific reports · 2020Article
- Long-Acting Glucagon-Like Peptide-1 Receptor Agonists Suppress Voluntary Alcohol Intake in Male Wistar Rats.Frontiers in neuroscience · 2020Article
- Repeated diazepam administration reversed working memory impairments and glucocorticoid alterations in the prefrontal cortex after short but not long alcohol-withdrawal periods.Cognitive, affective & behavioral neuroscience · 2018Article
- Role of GABAMolecular brain · 2017Review
- Article
- Synaptic targets: Chronic alcohol actions.Neuropharmacology · 2017Review
- Loss of δ-GABAAddiction biology · 2017Article
- Circadian Plasticity of Mammalian Inhibitory Interneurons.Neural plasticity · 2017Review
- The endocannabinoid system regulates synaptic transmission in nucleus accumbens by increasing DAGL-α expression following short-term morphine withdrawal.British journal of pharmacology · 2016Article
- Mechanisms of Neuroplasticity and Ethanol's Effects on Plasticity in the Striatum and Bed Nucleus of the Stria Terminalis.Alcohol research : current reviews · 2015Article
- Selective modulation of GABAergic tonic current by dopamine in the nucleus accumbens of alcohol-dependent rats.Journal of neurophysiology · 2014Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic alcohol exposure-induced changes in reinforcement mechanisms and motivational state are thought to contribute to the development of cravings and relapse during protracted withdrawal. The nucleus accumbens (NAcc) is a key structure of the mesolimbic dopaminergic reward system and plays an important role in mediating alcohol-seeking behaviors. Here we describe the long-lasting alterations of γ-aminobutyric acid type A receptors (GABA(A)Rs) of medium spiny neurons (MSNs) in the NAcc after chronic intermittent ethanol (CIE) treatment, a rat model of alcohol dependence. CIE treatment and withdrawal (>40 days) produced decreases in the ethanol and Ro15-4513 potentiation of extrasynaptic GABA(A)Rs, which mediate the picrotoxin-sensitive tonic current (I(tonic)), while potentiation of synaptic receptors, which give rise to miniature inhibitory postsynaptic currents (mIPSCs), was increased. Diazepam sensitivity of both I(tonic) and mIPSCs was decreased by CIE treatment. The average magnitude of I(tonic) was unchanged, but mIPSC amplitude and frequency decreased and mIPSC rise time increased after CIE treatment. Rise-time histograms revealed decreased frequency of fast-rising mIPSCs after CIE treatment, consistent with possible decreases in somatic GABAergic synapses in MSNs from CIE rats. However, unbiased stereological analysis of NeuN-stained NAcc neurons did not detect any decreases in NAcc volume, neuronal numbers, or neuronal cell body volume. Western blot analysis of surface subunit levels revealed selective decreases in α1 and δ and increases in α4, α5, and γ2 GABA(A)R subunits after CIE treatment and withdrawal. Similar, but reversible, alterations occurred after a single ethanol dose (5 g/kg). These data reveal CIE-induced long-lasting neuroadaptations in the NAcc GABAergic neurotransmission.
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