Journal
BIOLOGICAL PSYCHIATRY
Volume 65, Issue 8, Pages 646-653Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2008.10.042
Keywords
C57; DBA; dopamine; ethanol; plasticity; VTA
Categories
Funding
- State of California
- National Institutes of Health [R01 DA016782-04, F31 DA21464-01, T32 AA009455]
- Department of the Army [DAMD17-01-10736]
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Background: Genetic factors and previous alcohol experience influence alcohol consumption in both humans and rodents. Specifically, a prior experience with ethanol increases ethanol intake in both ethanol-preferring C57BL/6 (C57) and ethanol non-preferring DBA/2 (DBA) mice. Whereas the ventral tegmental area (VTA) importantly regulates dopamine levels and ethanol intake, it is unknown whether ethanol experience differentially alters synaptic properties of VTA dopamine neurons in ethanol-preferring and non-preferring mice. Methods: The properties of excitatory and inhibitory inputs and the ability to elicit long-term potentiation (LTP) were assessed with whole-cell patch-clamp recordings in VTA dopamine neurons from C57 and DBA mice 24 hours after a single ethanol (2 g/kg, IP) or equivalent saline injection. Results: Ethanol exposure increased gamma-aminobutyric acid (GABA) release onto VTA dopamine neurons in DBA mice, as previously observed in C57 mice. However, a single ethanol exposure reduced alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and N-methyl-D-aspartate receptor (NMDAR) function and LTP in VTA dopamine neurons from DBA but not C57 mice. Conclusions: A single ethanol exposure selectively reduced glutamate receptor function in VTA dopamine neurons from the ethanol non-preferring DBA strain but enhanced GABA signaling in both C57 and DBA strains. These results support the notion that VTA dopamine neurons are a central target of ethanol-induced neural plasticity, which could contribute to ethanol consumption. Furthermore, these findings highlight the possible need for specialized therapeutic interventions for alcoholism based on individual intrinsic differences.
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