Abstract
The present study investigated the role of the α1-containing GABAA receptors in the neurobehavioral actions of alcohol. In Experiment 1, mice lacking the α1 subunit (α1 (−/−)) were tested for their capacity to initiate operant-lever press responding for alcohol or sucrose. Alcohol intake in the home cage was also measured. In Experiment 2, the α1 (−/−) mice were injected with a range of alcohol doses (0.875–4.0 g/kg; i.p.) to evaluate the significance of the α1 subunit in alcohol's stimulant actions. In Experiment 3, we determined if the alcohol-induced stimulant effects were regulated via dopaminergic (DA) or benzodiazepine (BDZ)-dependent mechanisms. To accomplish this, we investigated the capacity of DA (eticlopride, SCH 23390) and BDZ (flumazenil, βCCt) receptor antagonists to attenuate the alcohol-induced stimulant actions. Compared with wild-type mice (α1 (+/+)), the null mutants showed marked reductions in both EtOH and sucrose-maintained responding, and home-cage alcohol drinking. The null mutants also showed significant increases in locomotor behaviors after injections of low–moderate alcohol doses (1.75–3.0 g/kg). βCCt, flumazenil, eticlopride, and SCH 23390 were able to attenuate the alcohol-induced stimulation in mutant mice, in the absence of intrinsic effects. These data suggest the α1 receptor plays an important role in alcohol-motivated behaviors; however, it also appears crucial in regulating the reinforcing properties associated with normal ingestive behaviors. Deleting the α1 subunit of the GABAA receptor appears to unmask alcohol's stimulatory effects; these effects appear to be regulated via an interaction of both DA- and GABAA BDZ-dependent mechanisms.
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Acknowledgements
This research was supported in part by grants AA10406 and AA11555 (HLJ) from the National Institute of Alcohol Abuse and Alcoholism (NIAAA), and grants GM52035 and GM47818 (GEH) from National Institute of General Medical Science (NIGMS). This work was also supported by MH 46851 (JMC) from the National Institute of Mental Health (NIH). Katrina Foster was supported in part by a Minority Neuroscience Fellowship from the American Psychological Association and the NIAAA Training Grant from the Indiana University School of Medicine (AA07462). We thank Dr Nicholas J Grahame for his outstanding consulting work on Experiments 1 and 2.
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June, H., Foster, K., Eiler, W. et al. Dopamine and Benzodiazepine-Dependent Mechanisms Regulate the EtOH-Enhanced Locomotor Stimulation in the GABAA α1 Subunit Null Mutant Mice. Neuropsychopharmacol 32, 137–152 (2007). https://doi.org/10.1038/sj.npp.1301097
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