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TRANSIENT CORTICAL ASTROGLIOSIS INDUCED BY ALCOHOL EXPOSURE DURING THE NEONATAL BRAIN GROWTH SPURT IN RATS
Citation:
Goodlett, C., J. Leo, J. Mahoney, J. West, AND J. O'Callaghan. TRANSIENT CORTICAL ASTROGLIOSIS INDUCED BY ALCOHOL EXPOSURE DURING THE NEONATAL BRAIN GROWTH SPURT IN RATS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/387 (NTIS PB95125605).
Description:
The astrocyte response to central nervous system injury induced by neonatal alcohol exposure was evaluated using radioimmunoassay and immunocytochemistry of glial fibrillary acidic protein (GFAP). at pups were exposed to alcohol on postnatal days 4 through 9 via artificial rearing. lcohol solutions were administered as one of the following treatments: 10.2% (v/V) in two feedings (4-5 g/kg/day), 5.1% (v/v) in four feedings (4.5 g/kg/day), or 2.5% (v/v) in 12 feedings (6.6 g/kg/day), producing mean blood alcohol concentrations (BACs) of approximately 300,180 and 50 mg/dl, respectively. ittermates were included as gastrostomy controls (GC) and suckle controls (SC). n postnatal day 10, GFAP concentration increased as a function of BAC, and the 10.2% alcohol treatment significantly and dramatically increased (TAP in the cortex (325% of SC). FAP immunocytochemistry revealed frequent loci of heavily labeled reactive astrocytes surrounding descending cortical blood vessels in the 10.2% group. n addition, a generalized increased in GFAP immunoreactivity was present in the deep layers of the cortex in all alcohol groups, marked by astrocytic fibrillary hypertrophy and increased density. hree-dimensional counts in layer V of parietal cortex using confocal microscopy indicated that the density of GFAP-labeled astrocytes of the 10.2% group was twice that of controls. he layer V gliosis was observable even at low BACS, while gliosis around the vasculature occurred only with high BACs, while gliosis around the vasculature occurred only with high BACs. y postnatal day 15, the astroglial effects were no longer evident.