Choline and DHA supplementation ameliorate hippocampal damage in prenatally stressed rats by reducing apoptosis and cortisol levels

Aim: Prenatal stress inhibits neurogenesis and increases apoptosis in the hippocampus. Both Choline [C] and docosahexaenoic acid [DHA] are essential nutrients, important for the formation of neural cell membrane phospholipid bilayer. The neuroprotective potential of synergistic supplementation of these nutrients on the outcome of hippocampal neural cell density and neural development in prenatally stressed gestation is seldom evaluated. This study assesses the role of supplemented choline and or DHA in prenatally stressed neonates on their hippocampal neural cell density and serum cortisol levels. Materials and Methods: Pregnant rat dams were separated into [NC] - Normal control, [SC] - Saline control, [STR] - Stress, [STR+C] - Stress+Choline, [STR+DHA] - Stress+DHA, and [STR+C+DHA] -Stress +Choline+DHA groups [n= 6/group]. NC dams were undisturbed throughout the gestation. All other experimental groups of dams were supplemented by Saline, C, and DHA throughout the gestation respectively. All STR group dams were exposed with restraint stress from E11 till delivery. On postnatal day 40, pups were sacrificed after blood sample collection to estimate cortisol levels. Results: Cresyl violet stained, and caspase-3 labeled hippocampal sections were observed to analysis neural cell density and apoptosis. Significant restoration (p<0.001) in the total number of viable neuronal cells in CA1and CA3 subregions of the hippocampus and reduced caspase-3 labeled apoptotic cells were observed in STR+C+DHA rat pups compared to the age-matched NC, SC and stressed pups. In addition, a significant reduction in (p<0.01) serum cortisol concentration was found in [STR+C+DHA] pups when compared with age-matched stressed rat pups. Conclusion: Oral supplementation of nutrition like choline and DHA during stress among rat dams restores stress induced neonate hippocampal neural cell density and diminishes apoptotic cells in CA1 and CA3 regions with reductions in serum cortisol levels.