A potential role for dendritic spines in bisphenol-A induced memory impairments during adolescence and adulthood.

Abstract

Developmental exposure to Bisphenol A (BPA), an endocrine disrupting chemical, alters many behaviors and neural parameters in rodents and non-human-primates. The effects of BPA are mediated via gonadal hormone, primarily, estrogen receptors, and are not limited to the perinatal period since recent studies show impairments further into development. The studies described in this chapter address the effects of BPA administration during early adolescence on memory and dendritic spine density in intact male and female rats as well as ovariectomized (OVX) rats in late adolescence and show that some of these adolescent induced changes endure into adulthood. In general, BPA impairs spatial memory and induces decreases in dendritic spine density in the hippocampus and the medial prefrontal cortex, two areas important for memory. The effects of adolescent BPA in intact females are compared to OVX females in an attempt to address the importance of estrogens in the mechanism(s) underlying the profound neuronal alterations occurring during adolescent development. In addition, potential mechanisms by which acute and chronic BPA induce structural alterations are discussed. These studies suggest a complex interaction between low doses of BPA, gonadal state and neural development.