Prenatal alcohol exposure decreases the number of nitric oxide synthase positive neurons in rat superior colliculus and periaqueductal gray

Abstract

Because nitric oxide (NO) is involved in the development and refinement of axonal projections and synapses, it is of interest to know if developmental alcohol exposures affect NO producing neurons. Pregnant rats were fed artificial liquid diet throughout gestation as the only fluid or caloric source. The diet for experimental dams contained ethanol (6.7% v/v) while the pair-fed diet for control dams contained isocaloric maltose–dextrin instead of ethanol. This ethanol diet regime is known to produce peak blood alcohol concentrations of approximately 140 mg%. Cells stained histochemically for nitric oxide synthase (NOS) were counted at postnatal day 15 (P15) and 35 (P35) in cross-sections of the stratum griseum superficiale (SGS) of the superior colliculus (SC) and in the dorsolateral column of the periaqueductal gray (dlPAG). Compared to control tissues, alcohol caused the following effects: In the SC, the areal density of NOS+ neurons was decreased 24% at P15 but a similar decrease in means at P35 was not statistically significant ( P=0.10); soma size was unaffected at either P15 or P35. In the dlPAG, both the areal density and the total number of NOS+ neurons per section were unaffected at P15 but were decreased at P35 (33% and 37% decreases); soma size was unaffected at either P15 or P35. The decrease in NOS+ neurons in the SC at P15 could be expected to have a negative impact on the refinement of neuronal connections while the decreases in NOS+ neurons in the dlPAG at P35 likely represent more permanent effects that could alter the function of that nucleus.