Exposure to ethanol (EtOH) during central nervous system (CNS) development can lead to a wide array of neuroanatomical, behavioral, and cognitive abnormalities, broadly subsumed under the fetal alcohol spectrum disorder classification. One mode of EtOH-induced interference in the normal developmental program appears to be through induction of apoptotic processes mediated by the Bcl-2 family of survival-regulatory proteins. The present series of studies investigated the role of the Bcl-2-related, pro-apoptotic Bid protein, and its truncated, apoptotically active fragment, tBid, in developmental EtOH neurotoxicity.
