Aims

To support the free and open dissemination of research findings and information on alcoholism and alcohol-related problems. To encourage open access to peer-reviewed articles free for all to view.

For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.

___________________________________________

Friday, February 1, 2008

Roles of the Nucleus Accumbens and Amygdala in the Acquisition and Expression of Ethanol-Conditioned Behavior in Mice
The Journal of Neuroscience, January 30, 2008, 28(5):1076-1084



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.

Read Full Abstract



Request Reprint E-Mail: gremelc@ohsu.edu
_____________________________________________________________