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Exposure to environmental contaminants poses a significant threat to normal growth and differentiation of the developing brain.1 As a member of the polycyclic aromatic hydrocarbon (PAH) family, B[a] P, is ubiquitous throughout the environment and is derived from the incomplete combustion of organic matter.2 It is known for its neurotoxic potential causing neurobehavioral alterations in animal models,3 and its metabolites can reach the brain tissues by crossing the blood-brain barrier and thereby gains direct access to the central nervous system.3–6 Accumulating evidence indicates that hippocampus is particularly important for spatial learning and memory,7 morphological changes occur during pregnancy, the postpartum period, and after weaning. However, in the present scenario very little is known about the mechanism of action and effects of these neurotoxicants on animals’ model inducing persistent cognitive dysfunction of offspring during early-life to result in diseased phenotypes in later-life. Although a various mode of administration were known an intraperitonial B[a] P administration during early gestation and the toxic insults induced by these neurotoxicants developing rat brain during postnatal development quite uncertain.

Prenatal exposure to Benzo[a]pyrene causes learning and memory impairment and loss of neurons in hippocampus during development of wistar rats