Lactational and postnatal exposure to polychlorinated biphenyls induces sex-specific anxiolytic behavior and cognitive deficit in mice offspring.

The central nervous system is affected by polychlorinated biphenyls (PCBs). Previous studies have indicated that developmental exposure to PCBs impairs behavioral performance and alters cognitive abilities. This study assessed the effects of lactational and postnatal exposure to a commercial PCBs mixture, Aroclor 1254 (A1254), on mice performing several neurobehavioral tasks including the open field test, novel object test, elevated plus maze test, Y-maze test, and tail suspension test. In the open field test, PCBs treatment (6 and 18 mg/kg/day) was associated with increased movement, time duration, and frequency in the central zone in female but not male mice. PCBs-treated female mice (6 and 18 mg/kg/day) also showed decreased novel object recognition, indicating impairment in recognition memory. Finally, we performed autoradiographic receptor binding assays for dopamine (DA) D₁ and D₂ receptors, dopamine transporter (DAT), and the N-methyl-D-aspartic acid (NMDA) receptor after behavioral tests to examine whether alterations occurred in the dopaminergic and NMDAergic systems of the brain. Our results showed that PCBs treatment did not change D₁ and D₂ receptors or DAT binding in the dorsal striatum of female mice. However, PCBs treatment significantly decreased NMDA receptor binding in the dorsal striatum, frontal cortex, cingulate cortex, and motor cortex, and CA3 and dentate gyrus (DG) of the hippocampus in female mice. Collectively, our results suggest that long-term PCBs exposure can induce anxiolytic behavior, cognitive deficits, and changes of NMDA receptors.