Neurodevelopment effects of early life bisphenol-A exposure on visual memory: Insights into recovery dynamics

Bisphenol A (BPA), a ubiquitous endocrine disruptor, is implicated in the cognitive deficits observed in both children and animals. Especially, BPA-induced spatial memory deterioration during the whole development phase of rodents has been well delineated. However, whether BPA exposure on the different development phases exerts similar effects on the prefrontal cortex (PFC) dependent visual memory is still elusive. Here, we chose two exposure windows, the whole gestation and lactation phases (E0∼P21) and the whole juvenile and adolescent phases (P22∼P60), for exposing rats to BPA. The visual memory of those rats was accessed by object recognition testing in the open field after BPA exposure and a constant recovery interval. The results revealed a substantial decline of visual memory under both exposure conditions, accompanied by an increase in anxiety-like behavior in BPA-exposed rats. Notably, after a 20-day recovery period, those behavioral changes induced by BPA exposure during P22∼60, not E0∼P21, were reversed compared to the control rats. According to morphological analysis of those rats after recovery, we found that the spine density of pyramidal neurons in the PFC were significant decreased in rats with BPA exposure during E0∼P21 and there was no difference between rats with or without BPA exposure during P22∼P60. Additionally, a similar change trend in excitatory receptors expression was observed under both exposure conditions. After an additional 20 days of recovery, the behavioral changes in rats with perinatal BPA exposure reverted to the normal status. Our present findings illuminate the dynamic effects of BPA on PFC-dependent functions across two crucial early developmental stages of life.