 Dr. George F. Koob, Ph.D. is Professor and Chairman of the Committee on the Neurobiology of Addictive Disorders at The Scripps Research Institute and Adjunct Professor of Psychology and Psychiatry and the Skaggs School of Pharmacy and Pharmaceutical Sciences at the University of California, San Diego. An authority on addiction and stress, his research interests include the neurobiology of emotion, with a focus on the theoretical constructs of reward and stress. He has made contributions to our understanding of the anatomical connections of the emotional systems and the neurochemistry of emotional function. His current research is focused on exploration of the neurobiological basis for the neuroadaptation associated with drug dependence and stress. He has published over 630 scientific papers, is the United States Editor-in-Chief of the journal Pharmacology Biochemistry and Behavior, Director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) Alcohol Research Center at The Scripps Research Institute, Director of the Pearson Center for Alcoholism and Addiction Research, and Consortium Coordinator for NIAAA's multi-center Integrative Neuroscience Initiative on Alcoholism. His awards include being honored as a Highly Cited Researcher from the Institute for Scientific Information, and the Distinguished Investigator, Mark Keller, and Tharp Awards from the Research Society on Alcoholism. |
| Abstract: Addiction has been conceptualized as a chronic relapsing disorder with roots in impulsivity and compulsivity, and neurobiological mechanisms change as the individual moves through the stages of the addiction cycle. Animal models of excessive drinking include binge models and models that focus on interactions with stress and dependence and include abstinence-induced drinking, drinking following abstinence and withdrawal, and drinking during protracted abstinence in animals with a history of dependence. Key neurochemical elements involved in reward and stress within a basal forebrain macrostructure termed the extended amygdala are hypothesized to be dysregulated in addiction to convey the vulnerability for compulsive drug intake. During intoxication, elements in the extended amygdala are activated. During the development of dependence, the reward systems become compromised, but there is also dysregulation of the brain stress systems such as corticotropin releasing factor, and norepinephrine and neuropeptide Y. In addition, critical neurocircuitry in the basal forebrain for cue-induced reinstatement are providing clues to the neurobiological basis of craving. Neurocircuitry involving separate components for craving, reward deficits, and compulsivity provide a heuristic framework for the study of individual differences in the vulnerability for addiction. |