Ethanol Modulates Glutamatergic Transmission and NMDAR-Mediated Synaptic Plasticity in the Agranular Insular Cortex
Open accessAbstract
The agranular insular cortex (AIC) has recently been investigated by the alcohol field because of its connectivity to and modulatory control over limbic and brainstem regions implicated in alcohol use disorder (AUD), and because it has shown involvement in animal models of alcohol drinking. Despite evidence of AIC involvement in AUD, there has not yet been an examination of whether ethanol modulates glutamatergic and γ-amino-butyric acid (GABA)ergic synaptic transmission and plasticity in the AIC. Characterizing how the synaptic transmission and plasticity states of AIC cortical processing neurons are modulated by acute ethanol will likely reveal the molecular targets by which chronic ethanol alters AIC function as alcohol drinking transitions from controlled to problematic. Therefore, we collected brain slices from ethanol-naïve adult male mice, obtained whole-cell recording configuration in layer 2/3 AIC pyramidal neurons, and bath-applied ethanol at pharmacologically relevant concentrations during electrophysiological assays of glutamatergic and GABAergic synaptic transmission and plasticity. We found that ethanol inhibited electrically evoked N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory postsynaptic currents (EPSCs) in a concentration-related fashion, and had little effect on evoked α-amino-3-hydrox-5-methylisoxazole-4-propionic acid-type receptor (AMPAR)-mediated EPSCs. Ethanol had no effect on spontaneous excitatory postsynaptic currents (sEPSCs) or inhibitory GABAAR-mediated postsynaptic currents (sIPSCs). We found that synaptic conditioning (low-frequency stimulation for 15 min at 1 Hz) induced a form of long-term depression (LTD) of evoked AMPAR-mediated EPSCs. The ability to induce LTD was inhibited by a nonselective NMDAR antagonist (DL-2-amino-5-phosphonovaleric acid), and also by acute, intoxicating concentrations of ethanol. Taken together these data suggest that the glutamate, but not GABA system in the AIC is uniquely sensitive to ethanol, and that in particular NMDAR-mediated processes in the AIC may be disrupted by pharmacologically relevant concentrations of ethanol.
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In vitro ethanol inhibits electrically-evoked NMDA receptor-mediated excitatory post-synaptic currents in brain slices of the aAgIC.
“In vitro ethanol inhibits electrically-evoked N-methyl-D-aspartate (NMDA) receptor-mediated excitatory post-synaptic currents (EPSCs) in brain slices of the aAgIC”
From The Insula: A Brain Stimulation Target for the Treatment of Addiction (2019) · cites this paper as Shillinglaw et al., 2018
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Synaptic Plasticity in the Agranular Insular Cortex Predicts Escalated Ethanol ConsumptionPreprint
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- Authors
- Shillinglaw, J. E., Morrisett, R. A., & Mangieri, R. A.
- Affiliations
- The University of Texas at Austin (US)
- Corresponding author
- Shillinglaw, Joel E.
- Mangieri, Regina A.
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2018-12-18
- Volume
- 9
- Pages
- 1458-1458
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC6305468
- OpenAlex
- W2904142135
- Cited by
- 21
- References
- 57
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 5 · 2020: 5 · 2019: 2
- FWCI
- 1.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (U24AA016651, R01AA015167)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- ethanol, agranular insular cortex, glutamatergic neurotransmission, NMDA receptor, synaptic plasticity, long-term depression, AMPA receptors, GABAergic neurotransmission, alcoholism, pyramidal neurons, layer 2/3
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