Adult Zebrafish (Danio rerio) Exposure to Bisphenol-A (BPA) Impairs Behavioral Lateralization

Cerebral lateralization describes the asymmetries between the two halves of the brain which results in side-specialized processing of certain functions. This phenomenon provides a selective advantage by promoting enhanced cognitive abilities. However, due to the plastic nature of lateralization, an individual’s lateralization is highly subject to change by many external factors, such as pollution, throughout its life. Additionally, lateralized regions are dependent on different contexts, so lateralized elements do not all experience the same effects. A common pollutant found worldwide is bisphenol-A (BPA), a critical component of many plastics. BPA is a known endocrine disruptor that can agonize and antagonize the functions of sex steroids. Other studies have demonstrated the importance of sex steroids in regulating the development of cerebral lateralization; BPA may similarly affect lateralization. A popular research animal for studying toxicology is the zebrafish. Its advantages include a fully sequenced genome, many human orthologs, and more importantly, expresses lateralized behaviors that are indicative of the strength of its cerebral lateralization. This experiment analyzed the effects of BPA exposure on visual lateralization of zebrafish. Given the role that sex steroids play in moderating lateralization, it was hypothesized that exposing zebrafish to BPA would diminish the strength of lateralization in the brain which would translate into reduced behavioral lateralization. To test this, one group was exposed to 0.01 mg/L BPA for one week and compared against a control group in their eye preference when approaching a visual cue. Two settings, a foraging context and a social context, were utilized to examine the scope of impairment in lateralization. The control group in both settings displayed similar strengths in behavioral lateralization with a left eye preference. However, the lateralized response faded completely with BPA treatment. This experiment demonstrates that BPA induces loss of lateralization and possesses similar impacts on mechanisms controlling investigatory behavior in these two contexts. Wild populations may encounter higher concentrations of BPA, and although there is greater variability in these exposures, this experiment proves that exposure even beyond critical periods of development can impair lateralization. Additional research will have to be conducted to identify the effects of BPA on other lateralized behaviors and sensory modalities to pinpoint the exact mechanisms through which BPA influences lateralization.