Gamma aminobutyric acid signaling disturbances and altered astrocytic morphology associated with Bisphenol A induced cognitive impairments in rat offspring.

Abstract

Bisphenol A (BPA) is a well-recognized endocrine disruptor and is globally used in the manufacture of many plastic items. Multiple studies suggest links between prenatal BPA exposure and alterations in neurodevelopment and behaviors in children, even at lower levels. This study was conducted to reveal the role of astrocyte morphology and Gamma aminobutyric acid (GABA) signaling in BPA induced cognitive defects in the offspring of Wistar albino rats when exposed during the prenatal and postnatal periods. Dams of Wistar albino rats were exposed to a dose of 5mg/kg body weight of BPA throughout the pregnancy and lactation period until the third postnatal day (PND). After delivery of pups, cognitive tests were carried out on the 21st, 24th, and 28th PNDs. Blood samples were collected for measurement of serum GABA levels. On the same day as the blood collections, pups were sacrificed and their right frontal cortices were dissected out. Immunohistochemical analysis for glial fibrillar acidic protein + astrocytes was conducted. Pre and postnatal BPA exposure led to anxiety like behavior in pups. This exposure also resulted in reduced serum GABA concentrations. Immunohistochemical analysis revealed reduced astrocyte numbers as well as decreased numbers of dendritic spines in the BPA exposed pups. BPA exposure during critical periods of development leads to cognitive impairments that correlate with the defects in the GABA signaling pathways and deteriorated morphology of the astrocytes in the offspring of the Wistar rats.