| Excessive consumption of ethanol during pregnancy can produce teratogenic effects in the developing brain, and can lead to the fetal alcohol syndrome (FAS). Previous studies have shown that, in the young postnatal guinea pig hippocampus, chronic prenatal ethanol exposure (CPEE) produces a decrease in the number of CA1 pyramidal cells by 25--30%. Functional deficits have also been reported, including a CPEE-induced decrease in the maximal excitatory post synaptic potential (EPSP) of the CA1 region of the hippocampus; and a reduction in chemically stimulated release of glutamate from hippocampal slices. These morphological and functional deficits may be a consequence of a CPEE-induced decrease in presynaptic innervation within the hippocampus. The presynaptic protein synaptosomal-associated protein of 25kDa (SNAP-25) is essential for synaptic vesicle fusion and neurotransmitter release, and its expression can be used to quantitate presynaptic innervation. The current study tested the hypothesis that CPEE leads to a change in SNAP-25 content in the guinea pig hippocampus. Timed, pregnant guinea pigs were treated with 4 g ethanol/kg maternal body weight/day, isocaloric-sucrose/pair-feeding, or water, throughout gestation. CPEE caused brain and hippocampal growth restriction in near-term fetal and adult guinea pigs. CPEE did not change SNAP-25 protein content in the hippocampus of the near-term fetal (GD 63: n = 3 litters) and adult (PD 60: n = 5 litters) guinea pig, as determined by immunoblot analysis and immunohistochemical analysis (PD 60--100: n = 5--7 litters). These findings suggest that changes in SNAP-25 protein expression do not precede or lead to CPEE-induced hippocampal cell loss. |
