Behavioral Plasticity After Teratogenic Alcohol Exposure as Recovery of Function
John H. Hannigan Wayne State University, Detroit
One long-term objective of our research has been to identify effective pharmacological or environmental treatments for the behavioral, attentional, and cognitive deficits commonly found in children with fetal alcohol syndrome (FAS) and alcohol-related birth defects (ARBDs; Abel, 1990; Streissguth, 1986). In complement to potential therapeutic value, analyses of differential behavioral responses to drug challenges could aid in the recognition and interpretation of neurobiological aspects of alcohol teratogenesis ( Hannigan & Blanchard, 1988). Among the wide range of fetal alcohol effects on central nervous system (CNS), we have chosen to study behavioral sequelae of dysfunctional forebrain dopamine systems and hippocampus. We initially agreed with reasoning that there was a dopaminergic dysfunction because rats exposed to alcohol prenatally tended to be overactive, and we first simplistically equated locomotor activity with dopamine activity ( Bond, 1986). We had also interpreted other behavioral outcomes as indicative of hippocampal dysfunction ( Riley, Barron, & Hannigan, 1986). This chapter reviews some of these neurobiological outcomes and our research on these systems after prenatal alcohol exposure, in terms of neurobehavioral plasticity.
FAS and ARBDs have been regarded the most common potentially preventable cause of mental retardation in Western countries ( Abel & Sokol, 1991). Given the widespread abuse of alcohol and the current difficulty in