PRENATAL COCAINE DELAYS ASTROGLIAL MATURATION - IMMUNODENSITOMETRY SHOWS INCREASED MARKERS OF IMMATURITY (VIMENTIN AND GAP-43) AND DECREASED PROLIFERATION AND PRODUCTION OF THE GROWTH-FACTOR S-100

Exposure to cocaine during fetal development has been demonstrated to produce a variety of brain and behavioral changes. Cocaine is a potent releaser of a variety of neurotransmitters, such as serotonin, which act as developmental signals. Since serotonin plays an important role in astroglial maturation, migration, and growth factor production (e.g . S-100 beta), we proposed that these properties of astroglial cells w ill be altered in a brain prenatally exposed to cocaine. To observe co caine's effects on astroglial development, we performed immunocytochem ical analyses of a variety of developmental protein markers including BrdU, Gap-43, vimentin, and S100 beta. Our results demonstrate that pr enatal cocaine administration produces decreased cell proliferation as measured by BrdU staining, retarded neurite outgrowth as ascertained by increased Gap-43 immunoreactivity, increased density of vimentin-po sitive radial glial cells, and diminished tissue S100 beta immunoreact ivity. Overall, these results suggest that cocaine delays astroglial d evelopment. This delay would have profound effects on neuronal develop ment and outgrowth and, thus, development of the entire brain.