Vulnerability of macaque cranial nerve neurons to ethanol is time- and site-dependent.

The present study tested the hypotheses that vulnerability to ethanol depends upon (1) population-based characteristics of the neuronal progenitors and (2) the maturation of that population by examining the effects of prenatal exposure to ethanol on brainstem nuclei derived from different rhombomeres and from the alar and basal plates. Macaca nemestrina received an ethanol-containing solution 1 day per week during the first 6 (Et6) or 24 (Et24) weeks of gestation. Control animals received an equivalent volume of saline. The treatment regime for some animals included early gastrulation (gestational day [G] 19 or G20), whereas others were treated later (on G21 or G24). Brainstems were cryosectioned and stained with cresyl violet. Stereological methods were used to determine the numbers of neurons in six different nuclei: the abducens, vagal, and hypoglossal motor nuclei and sensory components of the trigeminal brainstem nuclear complex (the principal, oral, and interpolar subnuclei). There were no differences in the numbers of neurons in any of the nuclei between controls and Et6-, or controls and Et24-treated monkeys. In contrast, the number of trigeminal sensory neurons was significantly (P<.05) lower in animals treated on G19/G20 than in control. No differences between controls and monkeys treated on G21/G24 were detected. No motor nuclei exhibited an ethanol-induced change. These data together with data on the trigeminal motor nucleus show that vulnerability to ethanol (1) is greater in sensory nuclei than in motor nuclei and (2) is temporally restricted to the time of gastrulation.