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Exploring the Role of Central Astrocytic Glutamate Uptake in Ethanol Reward in Mice
Author(s) -
Smith Karen L.,
John Catherine S.,
Sypek Elizabeth I.,
Öngür Dost,
Cohen Bruce M.,
Barry Sarah M.,
Bechtholt Anita J.
Publication year - 2014
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12361
Subject(s) - glutamate receptor , glutamatergic , conditioned place preference , ethanol , neuroscience , binge drinking , astrocyte , alcohol , context (archaeology) , psychology , endocrinology , pharmacology , medicine , central nervous system , chemistry , dopamine , biochemistry , biology , alcohol consumption , paleontology , receptor
Background Alcoholism is associated with specific brain abnormalities revealed through postmortem studies, including a reduction in glial cell number and dysregulated glutamatergic neurotransmission. Whether these abnormalities contribute to the etiology of alcoholism, are consequences of alcohol use, or both is still unknown. Methods We investigated the role of astrocytic glutamate uptake in ethanol (Et OH ) binge drinking in mice, using the “drinking in the dark” ( DID ) paradigm by blocking the astrocytic glutamate transporter ( GLT ‐1) with intracerebroventricular ( ICV ) administration of dihydrokainic acid ( DHK ). To determine whether astrocytic glutamate uptake regulates the conditioned rewarding effects of Et OH , we examined the effects of ICV DHK on the acquisition and expression of Et OH ‐induced conditioned place preference. Results Blocking central astrocytic glutamate uptake selectively attenuated Et OH binge drinking behavior in mice. DHK did not alter the acquisition or expression of preference for Et OH ‐associated cues, indicating that reduced astrocytic glutamate trafficking may decrease binge‐like drinking without altering the conditioned rewarding effects of Et OH . Conclusions Several alternative conclusions are plausible, however, interpreting these data in the context of the human literature, these findings suggest that the reduction of glia in the alcoholic brain may not be a predisposing factor to developing alcoholism and could be a consequence of Et OH toxicity that decreases excessive Et OH intake.