Neuropeptide Y expression confers benzo[a]pyrene induced anxiolytic like behavioral response during early adolescence period of male Wistar rats

Environmental neurotoxicant like benzo[a]pyrene (B[a]P) is known to induce neurobehavioral changes. Our previous reports address the adverse effect of B[a]P on the neurobehavioral responses and neuromorphology of sensitive brain regions in adolescent rats. Present study was conducted on male Wistar rat neonates at postnatal day 5 (PND5) to ascertain B[a]P induced anxiolytic like behavioral response could be an outcome of neuropeptide Y (NPY) overexpression in brain. Single intracisternal administration of B[a]P was carried out at PND5 to elucidate the role of NPY on neurobehavioral responses at PND30. The behavioral studies showed anxiolytic like effect of B[a]P in both light and dark box and elevated plus maze tests. Antioxidant assay involving glutathione peroxidase activity was significantly decreased where as lipid peroxidation was significantly augmented in both hippocampus and hypothalamus of B[a]P treated group as compared to naive and control. The neurotransmitter estimation by HPLC-ECD showed significant increase in 5-HT level in both hippocampus and hypothalamus of B[a]P treated group. Significant elevation in NPY expression was observed in both hippocampus and hypothalamus of B[a]P group. Intracellular Ca2 + estimation using Fura-2AM by fluorometry showed that B[a]P induced increase in Ca2 + influx was associated with augmented NPY expression in brain. As NPY has orexigenic effect, our result revealed that there was a significant increase in body weight at PND30 following B[a]P administration to rat neonates at PND5. These findings suggested that NPY overexpression in brain regions might be associated with anxiolytic like behavioral response and orexigenic effect in rats following single intracisternal B[a]P administration. Future research directing towards understanding the signaling cascades of B[a]P induced biochemical and neuromorphological alteration might address the independent pathway which induce neurodegeneration despite NPY overexpression in brain regions of adolescent rats.