This work was supported by the National Institute on Alcohol Abuse and Alcoholism Grants AA06420 and AA08459. This is publication no. 9704-NP of The Scripps Research Institute.
Intra-amygdala Muscimol Decreases Operant Ethanol Self-administration in Dependent Rats
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 20, Issue 7, pages 1289–1298, October 1996
How to Cite
Roberts, A. J., Cole, M. and Koob, G. F. (1996), Intra-amygdala Muscimol Decreases Operant Ethanol Self-administration in Dependent Rats. Alcoholism: Clinical and Experimental Research, 20: 1289–1298. doi: 10.1111/j.1530-0277.1996.tb01125.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication January 11, 1996; accepted June 10, 1996
Dependence is an important factor motivating continued alcohol use in human alcoholics. Development of a model of ethanol (EtOH) consumption in dependent animals would advance the understanding of reinforcement after chronic EtOH exposure and allow for the investigation of the neuropharmacological mechanisms mediating reinforcement in dependent versus nondependent animals. In the present study, rats were trained to lever press for 10% EtOH, surgically implanted with bilateral guide cannulae in the amygdala, and either made dependent on EtOH by exposure for 2 weeks to EtOH or exposed to air in identical vapor chambers. Upon removal, the rats were placed in operant boxes and allowed to respond on levers for 10% EtOH or water during a 12-hr period. Rats were removed briefly at ∼6.5 hr for intra-amygdala injections of saline or the GABAA, receptor agonist muscimol. After the test period, rats were returned to the vapor Chambers for 4 days before retest. EtOH-dependent animals responded more for EtOH across the 12-hr test period than did air control nondependent rats; this difference became more pronounced with repeated test sessions. Intra-amygdala muscimol significantly decreased responding for EtOH in EtOH-dependent rats, but had no effect in nondependent controls. These data suggest that the reinforcing effects of EtOH and neurotransmitter pathways mediating reward are altered after the development of dependence, and they support the use of this paradigm for further investigations into the neuropharmacology of EtOH dependence.