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111. Pre-Congress: July 2, 20051.1. Animal Models of Addiction: Relevance for Understanding the Neurobiology ofAddictionGeorge Koob, Scripps Research Institute, La Jolla, USA (gkoob@ucsd.edu)Drug addiction has been conceptualized as compulsive drug taking with a loss of control over intake thatreflects an impulse control disorder beginning with positive reinforcement and shifting to a compulsivedisorder with negative reinforcement. Under this framework, drug addiction is composed of threecomponents: a binge/intoxication stage, a withdrawal-negative affect stage, and apreoccupation/anticipation (craving) stage. Animal models for various stages of the drug abuse cycle havebeen developed and are providing a rational basis for our understanding of the neurobiology of addiction.Animal models of the binge/intoxication stage include drug self-administration, place preference, brainreward thresholds, and escalated drug intake associated with extended access. Animal models for thewithdrawal/negative affect stage include place aversions and brain reward threshold measures. Animalmodels for the preoccupation/anticipation (craving) stage include drug-, stress- and cue-inducedreinstatement and drug taking following abstinence and withdrawal. Common neurobiological elementsthat follow the shift from impulsive to compulsive dysregulation in drug addiction include compromisedbrain reward and stress systems and is comprised of key elements of a basal forebrain macrostructuretermed the extended amygdala and its connections. Neuropharmacologic studies in animal models ofaddiction have provided evidence for the dysregulation of specific neurochemical mechanisms in specificbrain reward systems in the extended amygdala (opioid peptides, γ-aminobutyric acid, glutamate anddopamine). There also is recruitment of brain stress systems (corticotropin-releasing factor andnorepinephrine) and dysregulation of brain anti-stress systems (neuropeptide Y) that provide the negativemotivational state associated with drug abstinence. The changes in the reward and stress systems arehypothesized to maintain hedonic stability in an allostatic state, as opposed to a homeostatic state, and assuch convey the vulnerability for development of dependence and relapse in addiction. Future challengescenter on identifying the molecular and cellular changes that contribute to the neuroadaptations withinspecific motivationally relevant neurocircuits associated with transition to dependence, motivationalwithdrawal, protracted abstinence and vulnerability to relapse.1.2.Processing of Reward Information by Dopamine Neurons and Other Brain StructuresWolfram Schultz, Cambridge University (ws234@cam.ac.uk)Information about rewards is processed in a number of brain structures, such as the dopamine system,striatum and orbitofrontal cortex. We found in formal learning paradigms that dopamine neurons detect theextent to which rewards occur differently than predicted, thus coding an 'error' in the prediction of reward.Together with their anatomical organization and influence on postsynaptic structures, dopamine neuronsmay thus serve as explicit teaching signals mediating changes in immediate responses and learning.Neurons in the orbitofrontal cortex discriminate well between different rewards irrespective of the positionsand objects of the stimuli predicting them and may serve as a highly sensitive reward-discriminatingsystem. Neurons in the striatum incorporate reward information into activity related to the preparation andexecution of movements leading to the reward, thus possibly reflecting a neural mechanism underlying