Reduced alcohol intake and reward associated with impaired endocannabinoid signaling in mice with a deletion of the glutamate transporter GLAST
Open accessAbstract
A hyperglutamatergic state has been hypothesized to drive escalation of alcohol intake. This hypothesis predicts that an impairment of glutamate clearance through inactivation of the astrocytic glutamate transporter, GLAST (EAAT1), will result in escalation of alcohol consumption. Here, we used mice with a deletion of GLAST to test this prediction. WT and GLAST KO mice were tested for alcohol consumption using two-bottle free-choice drinking. Alcohol reward was evaluated using conditioned place preference (CPP). Sensitivity to depressant alcohol effects was tested using the accelerating rotarod, alcohol-induced hypothermia, and loss of righting reflex. Extracellular glutamate was measured using microdialysis, and striatal slice electrophysiology was carried out to examine plasticity of the cortico-striatal pathway as a model system in which adaptations to the constitutive GLAST deletion can be studied. Contrary to our hypothesis, GLAST KO mice showed markedly decreased alcohol consumption, and lacked CPP for alcohol, despite a higher locomotor response to this drug. Alcohol-induced ataxia, hypothermia, and sedation were unaffected. In striatal slices from GLAST KO mice, long-term depression (LTD) induced by high frequency stimulation, or by post-synaptic depolarization combined with the l-type calcium channel activator FPL 64176 was absent. In contrast, normal synaptic depression was observed after application of the cannabinoid 1 (CB1) receptor agonist WIN55,212-2. Constitutive deletion of GLAST unexpectedly results in markedly reduced alcohol consumption and preference, associated with markedly reduced alcohol reward. Endocannabinoid signaling appears to be down-regulated upstream of the CB1 receptor as a result of the GLAST deletion, and is a candidate mechanism behind the reduction of alcohol reward observed.
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Alterations in astrocytic glutamate clearance occur in schizophrenia and other psychiatric illnesses, and mice with GLAST deletion show phenotypic abnormalities such as mental and behavioral deficits.
“Alterations in astrocytic glutamate clearance are known to occur in schizophrenia and other psychiatric illnesses, and mice with glutamate/aspartate transporter (GLAST) deletion show phenotypic abnormalities such as mental and behavioral deficits. 90 , 91”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [91]
The Introduction identifies GLAST as an astrocytic transporter involved in glutamate clearance, and the Discussion and Results report altered alcohol reward and locomotor responses in GLAST-knockout mice. The paper does not report altered astrocytic glutamate clearance in schizophrenia or other psychiatric illnesses, and it does not establish general mental deficits; Results §3.3 finds no general impairment of associative learning. No page numbers were available in our copy. (LLM, conf=0.85)
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Orsolini, L., Longo, G., Giordano, M., & Volpe, U. (2026) · Advances in experimental medicine and biology · doi:10.1007/978-981-95-6872-7_15
- Authors
- Karlsson, R.-M., Adermark, L., Molander, A., Perreau-Lenz, S., Singley, E., Solomon, M., Holmes, A., Tanaka, K., Lovinger, D. M., Spanagel, R., & Heilig, M.
- Affiliations
- National Institutes of Health (US)
- University of Mannheim (DE)
- Tokyo Medical and Dental University (JP)
- Corresponding author
- Heilig, Markus
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2012-08
- Volume
- 63
- Issue
- 2
- Pages
- 181-189
- ISSN
- 0028-3908 (ISSN-L)
- PMC
- PMC3372600
- OpenAlex
- W2039211605
- Cited by
- 44
- References
- 56
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 3 · 2022: 2 · 2021: 2 · 2019: 5 · 2018: 1 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 3
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- amfAR, The Foundation for AIDS Research
- Novartis Foundation
- Bundesministerium für Bildung und Forschung
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (ZIAAA000487)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- GLAST, alcohol consumption, alcohol reward, endocannabinoid signaling, CB1 receptor, astrocytes, glutamate clearance, long-term depression, corticostriatal pathway
- MeSH terms
- Alcohol Drinking, Ethanol, Animals, Association Learning, Choice Behavior, Conditioning, Classical, Neuronal Plasticity, Reward, Signal Transduction, Mice, Knockout, Excitatory Amino Acid Transporter 1, Mice, Endocannabinoids
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