NEUROCIRCUITRY TARGETS IN ETHANOL REWARD AND DEPENDENCE

Alcoholism is a complex behavioral disorder characterized by excessive consumption of ethanol, a narrowing of the behavioral repertoire towa rd excessive consumption, the development of tolerance and dependence, and impairment in social and occupational functioning. Animal models of the complete syndrome of alcoholism are difficult if not impossible to achieve, but validated animal models exist for many of the differe nt components of the syndrome. Recent work has begun to define the neu rocircuits responsible for the two major sources of reinforcement key to animal models of excessive ethanol intake: positive and negative re inforcement. Ethanol appears to interact with ethanol-sensitive elemen ts within neuronal membranes that convey the specificity of neurochemi cal action. Ethanol reinforcement appears to be mediated by an activat ion of GABA-A receptors, release of opioid peptides, release of dopami ne, inhibition of glutamate receptors, and interaction with serotonin systems. These neurocircuits may be altered by chronic ethanol adminis tration as reflected by opposite effects during acute ethanol withdraw al and by the recruitment of other neurotransmitter systems such as th e stress neuropeptide corticotropin-releasing factor. Future challenge s will include a focus on understanding how these neuroadaptive change s convey vulnerability to relapse in animals with a history of ethanol dependence.