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Accumbens neurochemical adaptations produced by binge-like alcohol consumption

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Abstract

Rationale

The Scheduled High Alcohol Consumption (SHAC) binge drinking model is a simple, partial murine model with which to investigate some of the neurobiological underpinnings of alcoholism.

Objectives

The SHAC model was used to characterize monoamine and amino acid adaptations produced in the nucleus accumbens (NAC) by repeated bouts of high alcohol consumption.

Methods

In vivo microdialysis was conducted in the NAC of C57BL/6J (B6) mice during consumption of water, a 5% alcohol (v/v) solution for the first time (SHAC1) or a 5% alcohol solution for the sixth time (SHAC6). A second set of microdialysis experiments assessed the neurotransmitter response to an alcohol challenge injection (1.5 or 2 g/kg, IP).

Results

In both drinking experiments, SHAC1 and SHAC6 mice consumed comparable amounts of alcohol during the 40-min period of alcohol availability (~1.5 g/kg) and total fluid intake was similar between water and SHAC1/6 mice. Despite the similarity in alcohol consumption, alcohol-mediated increases in the extracellular concentration of GABA and serotonin were reduced, but glutamate was increased in the NAC of SHAC6 mice, relative to SHAC1 animals. No differences were observed in extracellular dopamine between SHAC1 and SHAC6 mice during alcohol consumption. After alcohol injection, SHAC6 mice also exhibited sensitized glutamate release, but did not differ from water or SHAC1 animals for any of the other neurotransmitters examined. Brain alcohol concentrations did not differ between groups after injection.

Conclusions

Repeated bouts of high alcohol consumption induce an imbalance between inhibitory and excitatory neurotransmission within the NAC that may drive excessive drinking behavior.

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Acknowledgements

This work was supported by NIAAA grants AA-013517 (INIA West) and AA-015351 to KKS.

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Correspondence to Karen K. Szumlinski.

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Szumlinski, K.K., Diab, M.E., Friedman, R. et al. Accumbens neurochemical adaptations produced by binge-like alcohol consumption. Psychopharmacology 190, 415–431 (2007). https://doi.org/10.1007/s00213-006-0641-7

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  • DOI: https://doi.org/10.1007/s00213-006-0641-7

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