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
C. Clarke et al., 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, Developmental brain research, 91(2), 1996, pp. 268-273
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.