Fetal alcohol and maternal stress modify the expression of proteins controlling postnatal development of the male rat hippocampus.

Background: Developing brains can partially get over prenatal alcohol exposure-related detrimental conditions by activating some mechanisms involved in survival. Objectives: This study aimed to shed light on the molecular correlates of compensatory mechanisms by examining temporal profiles in the expression of proteins controlling postnatal development in the rat hippocampus prenatally exposed to intubation stress/ethanol. Methods: Male pups were randomly assigned to age subgroups (n = 21/age) which were sacrificed on postnatal day (PD)1, PD10, PD30, and PD60. Ethanol (6 g/kg/day) were intragastrically intubated to the dams throughout 7-21 gestation days. The expression of neurogenesis and angiogenesis markers, extracellular matrix proteins, and growth-promoting ligands were examined by western blot. Results: The most rapid increase in the index of neuronal maturation was noted between PD10-PD30 (p < .05). Prenatal stress caused a decrease of neurogenesis markers at birth and an increase of their expressions at PD10 and PD30 to reach control levels (p < .001). The impact of fetal-alcohol was observed as a decrease in the expression of synaptic plasticity protein versican at birth (p < .001), an increase in the synaptic repulsion protein ephrin-B2 at PD10 (p < .001), and a decrease in the maturation of BDNF at PD30 (p < .001) with a decrease in the mature neuron markers at PD30 (p < .001) and PD60 (p = .005) which were compensated with upregulation of angiogenesis and increasing brevican expression, a neuronal maturation protein (p < .001). Conclusion: These data provide in vivo evidence for the potential therapeutic factors related to neurogenesis, angiogenesis, and neurite remodeling which may tolerate the alcohol/stress dependent teratogenicity in the developing hippocampus.