Heaton Marieta Barrow, Paiva Michael, Mayer Joanne, Miller Rehae
Department of Neuroscience, McKnight Brain Institute, University of Florida College of Medicine, Gainesville, FL 32610-0244, USA.
Neurosci Lett. 2002 Dec 13;334(2):83-6. doi: 10.1016/s0304-3940(02)01123-0.
The neonatal cerebellum undergoes an early period of ethanol sensitivity in which profound neuronal loss is seen following acute exposure, while slightly later exposure produces no such loss. This study was designed to determine whether this differential susceptibility is related to differences in ethanol-induced generation of reactive oxygen species (ROS). We found that ethanol treatment on postnatal day 4 (P4), the peak period of cerebellar vulnerability, resulted in ROS increases, but slightly later exposure (on P7) produced no immediate changes in ROS, but reductions were seen at 12 and 24 h following exposure. Exposure on P14 produced consistent decreases in ROS production. Thus, differential responsiveness in oxidative processes may play a major role in the differential temporal ethanol vulnerability of developing cerebellum.
