Abstract
Bisphenol-A (BPA) is a monomer used in the production of polycarbonate plastics, epoxies and resins and is present in many common household objects ranging from water bottles, can linings, baby bottles, and dental resins. BPA exposure has been linked to numerous negative health effects throughout the body, although the mechanisms of BPA action on the developing brain are still poorly understood. In this study, we sought to investigate whether low dose BPA exposure during a developmental phase when brain connectivity is being organized can cause long-term deleterious effects on brain function and plasticity that outlast the BPA exposure. Lactating dams were orally exposed to 25 μg/kg/day of BPA (one half the U.S. Environmental Protection Agency’s 50 μg/kg/day rodent dose reference) or vehicle alone from postnatal day (P)5 to P21. Pups exposed to BPA in their mother’s milk exhibited deficits in activity-dependent plasticity in the visual cortex during the visual critical period (P28). To determine the possible mechanisms underlying BPA action, we used immunohistochemistry to examine histological markers known to impact cortical maturity and developmental plasticity and quantified cortical dendritic spine density, morphology, and dynamics. While we saw no changes in parvalbumin neuron density, myelin basic protein expression or microglial density in BPA-exposed animals, we observed increases in spine density on apical dendrites in cortical layer five neurons but no significant alterations in other morphological parameters. Taken together our results suggest that exposure to very low levels of BPA during a critical period of brain development can have profound consequences for the normal wiring of sensory circuits and their plasticity later in life.
Highlights
There is growing public awareness of the possible health impact of exposure to environmental toxicants
We chose to focus on a well described form of activity-dependent plasticity which is robustly elicited in the rodent binocular visual cortex following 4-day monocular deprivation (4d MD) during the visual critical period (Hubel and Wiesel, 1970)
To determine how BPA exposure affects cortical synaptic plasticity, lactating dams were fed a vanilla cookie impregnated with either 25 μg/kg/day BPA or oil daily during the period that their pups were postnatal day 5 (P5) to P21. Animals had their contralateral eye monocular deprived on P28 and were assayed for ocular dominance plasticity (ODP) using intrinsic signal imaging on P32 (Figure 1A; No MD BPA-early, 4d MD BPA-early; Figure 1B, top panel). Notice that in this early exposure paradigm, the animals experience BPA during a developmental window which encompasses a period of rapid synaptogenesis and circuitry development, but that exposure ends a week before plasticity is induced
Summary
There is growing public awareness of the possible health impact of exposure to environmental toxicants. One of the most ubiquitous of these is bisphenol-A (BPA), a monomer used in the production of consumer materials such as water and baby bottles (Brede et al, 2003), can linings (Kang et al, 2003), and dental sealants (Suzuki et al, 2000; Joskow et al, 2006). Processes such as heat and pH level shifts are sufficient to trigger BPA migration out of everyday household items and into the surrounding environment (Kang et al, 2003). Numerous studies on BPA exposure have described adverse outcomes with much lower doses than the EPA standard (Itoh et al, 2012; Rochester, 2013; Szychowski and Wojtowicz, 2013)
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