Substance Abuse: Issues and Current Research
Thursday, 2:30 PM - 4:15 PM
Sheraton Constitution A&B

Chair: Laurie Chassin, Arizona State University

Presentation 1
Drug Addiction: A Brain Developmental Disorder
Speaker: Nora Volkow, National Institute on Drug Abuse, National Institutes of Health

Biographical Sketch
Nora D. Volkow, M.D., was appointed Director of the National Institute on Drug Abuse (NIDA) in May 2003. She is recognized as one of the world’s leading experts on drug addiction and brain imaging. Dr. Volkow’s work has been pivotal in demonstrating that drug addiction is a disease of the brain. She pioneered the use of brain imaging to investigate the toxic effects of drugs and the effects of drugs responsible for their addictive properties in the human brain. In addition, she has made important contributions to the neurobiology of obesity, to the neurobiology of the behavioral changes that occur with aging, and to the treatment of ADHD.

Abstract
Recent research supports the notion that addiction is a complex brain developmental disorder that often has its beginnings in childhood and adolescence, a period of dramatic change in brain structure and function. The relative vulnerability of the brain during the transition from childhood to adulthood may explain the heightened propensity of adolescents to act impulsively and to ignore the negative consequences of their behavior, both of which increase the risk for self-administration of drugs and for substance abuse at this stage of development. Since drugs of abuse interact with a number of neurotransmitter systems essential in brain development, exposure during the adolescent period may be particularly harmful to the still-developing brain. The presence of a mental disorder further increases an adolescent’s risk of drug abuse and addiction and poses an added challenge to their prevention and treatment. This presentation will highlight recent evidence demonstrating the impact drugs of abuse can have on the adolescent prefrontal cortex and other areas of the brain critical to memory, impulse control and decision-making as well as the implications these findings have for developing effective prevention and treatment strategies.

Presentation 2
Adolescence-Typical Alcohol Sensitivities and Intake
Speaker: Linda Spear, Binghamton University

Biographical Sketch
Linda Spear is Distinguished Professor of Psychology at Binghamton University, received Ph.D. training in Psychology and postdoctoral training in Neuroscience at the University of Florida. Dr. Spear has published over 180 peer-reviewed publications in the areas of developmental psychobiology, psychopharmacology, and toxicology, including a widely cited review of adolescent brain and behavioral function (Spear, 2000). Areas of particular expertise include adolescent sensitivity to ethanol, the neurobiology of risk taking and the contribution of adolescent-relevant motivational strategies, alcohol/drug use and peer affiliations to risk taking, impulsivity, and other problem behaviors of adolescence. Her research examining fundamental characteristics of adolescence using animal models is currently supported by grants from NIDA and NIAAA, including a MERIT award from NIAAA. She is the 2005 recipient of the Keller Award, an award given annually by NIAAA to “an outstanding alcohol researcher who has made significant and long-term contributions” to the study of alcohol abuse and alcoholism.

Abstract
The brain undergoes considerable sculpting during adolescence. These neural transformations have been highly conserved evolutionarily and are associated with a variety of adolescent-typical behavior patterns, including an elevated propensity to use, sometimes excessively, alcohol and other drugs. One possible contributor to the increased ethanol consumption often seen during adolescence in humans as well as various animal models is age differences in ethanol sensitivity and tolerance. Indeed, research conducted in laboratory animals has shown adolescents to be less sensitive than adults to many intoxicating effects of ethanol (e.g., ethanol-induced motor impairment, dysphoria and sedation) that presumably serve as cues to terminate intake. Adolescents are conversely more sensitive than adults to a few restricted effects of ethanol, including ethanol-induced social facilitation and impairments in memory and long-term-potentiation. Although ethical constraints limit conduct of comparable studies in humans, there are intriguing hints that similar ontogenetic patterns of ethanol sensitivities may be seen in human adolescents as well. These age-specific ethanol sensitivities are not simply related to pharmacokinetic factors, but appear to reflect differential rates of ontogeny of neural systems underlying different effects of ethanol, as well as a marked ontogenetic decline in expression of within session tolerance (acute tolerance). A decreased sensitivity of adolescents to ethanol, perhaps when exacerbated further by attenuated ethanol sensitivities associated with genetic risk and the tolerance emerging from prior ethanol use, may permit relatively high levels of alcohol intake among vulnerable adolescents, increasing their risk for alcohol abuse disorders.