Acute and long-term changes in the cerebellum following developmental exposure to ethanol.

Ethanol exposure during development can lead to structural damage to the cerebellum with associated behavioral dysfunction. Deficits in cerebellar weight and Purkinje cell number in the cerebellum of the rat are a function of the timing of the exposure and the peak blood alcohol concentration (BAC). Purkinje cell loss is greater following exposure during the third trimester equivalent than during the second trimester equivalent. Interestingly, Purkinje cells switch rapidly from being highly vulnerable on postnatal days 4 and 5 to being much more resistant after postnatal day 7. Furthermore, the higher the peak BAC, the more severe the deficits. Both in vivo and in vitro studies indicate that alcohol can kill postmitotic cells in a dose-dependent manner. Ethanol exposure that produces neuronal deficits also produces associated behavioral dysfunction, including deficits in balance. The mechanisms responsible for these changes are unknown, but the likelihood of ethanol-induced structural and functional damage during development is associated with both regional and temporal vulnerability and to the peak BAC.