ACUTE AND LONG-TERM NEURONAL DEFICITS IN THE RAT OLFACTORY-BULB FOLLOWING ALCOHOL EXPOSURE DURING THE BRAIN GROWTH SPURT

This study demonstrates that there is a relative recovery in the number of olfactory bulb granule cells following an initial alcohol-induced deficit, while the number of mitral cells remains permanently and severely depressed. The importance of pattern of exposure in influencing the severity of alcohol-induced neuronal loss in the olfactory bulb is also demonstrated. Sprague-Dawley rat pups were reared artifically and were administered alcohol over postnatal days (PD) 4 through 9, a period of rapid brain growth comparable to part of the human third trimester. Two groups received a daily alcohol dose of 4.5 g/kg, administered either as a 5.1% or 10.2% solution. A third group received a higher daily alcohol dose of 6.6 g/kg administered continuously as a 2.5% solution. Pups were either sacrificed on PD 10 or were allowed to grow to adulthood and sacrificed on PD 90. The number of mitral cells and granule cells and the area of the subependymal zone were determined from single sections. On PD 10, immediately following the alcohol exposure, both the mitral cells and the granule cells were significantly reduced in number, relative to controls, in both of the groups receiving the concentrated (5.1% and 10.2%) alcohol treatments. On PD 90, however, only the mitral cell number remained significantly reduced in the groups receiving the concentrated solutions, while the number of granule cells no longer differed significantly from that of controls. The group receiving the higher daily dose (6.6 g/kg) in continuous fractions had no significant cell loss at 10 or 90 days of age. There was no significant effect of any treatment or at any age on the area of the subependymal zone. These results suggest that the acute and long-term effects of alcohol on neuronal number vary among neuronal populations and that compensatory changes may occur in some neuronal complements following cessation of the alcohol exposure.