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The Journal of Neuroscience, January 30, 2008, 28(5):1076-1084; doi:10.1523/JNEUROSCI.4520-07.2008

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Behavioral/Systems/Cognitive
Roles of the Nucleus Accumbens and Amygdala in the Acquisition and Expression of Ethanol-Conditioned Behavior in Mice

Christina M. Gremel and Christopher L. Cunningham

Department of Behavioral Neuroscience and Portland Alcohol Research Center, Oregon Health & Science University, Portland, Oregon 97239-3098

Correspondence should be addressed to Christina M. Gremel, Department of Behavioral Neuroscience, L470, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098. Email: gremelc{at}ohsu.edu

Although progress has been made identifying the neural areas underlying the primary reinforcing effects of ethanol, few studies have examined the neural areas mediating ethanol-induced conditioned effects. Previous work using the conditioned place preference (CPP) procedure implicates the ventral tegmental area (VTA) (Bechtholt and Cunningham, 2005), but the downstream neural areas modulating the conditioned rewarding effects of ethanol have not been identified. Although the nucleus accumbens (Acb) and the amygdala (Amy), which both receive dopamine innervation from the VTA, have been implicated in the primary reinforcing effects of ethanol, the roles these areas play in ethanol-conditioned behaviors are unknown. In the present set of experiments, we use the CPP procedure along with selective electrolytic lesions to examine the neural areas underlying the acquisition and expression of ethanol conditioned behavior. In the acquisition experiment, male DBA/2J mice received bilateral lesions of the Acb or Amy before CPP training. In the expression experiments, mice received bilateral lesions of the Acb, Acb shell, Acb core, and Amy, or unilateral lesions of the Amy after training but before testing. Lesions of the Acb and Amy before training disrupted acquisition and expression of ethanol CPP. However, when given after training, only lesions of the Amy disrupted expression, whereas lesions of the Acb core facilitated loss of responding, of ethanol CPP. For the first time, these results demonstrate the role of the Acb and Amy in the acquisition and expression of ethanol-induced conditioned reward.

Key words: conditioned place preference; conditioned reinforcement; locomotor activity; lesion; inbred mice (DBA/2); accumbens

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Received June 13, 2007; revised Dec. 4, 2007; accepted Dec. 5, 2007.

Correspondence should be addressed to Christina M. Gremel, Department of Behavioral Neuroscience, L470, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098. Email: gremelc{at}ohsu.edu

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