PURPOSE: Bisphenol A (BPA), a common environmental endocrine disrupter, has been implicated in the induction of anxiety-like behavior and decrease of synaptic plasticity in amydala, mPFC and hippocampus. The neural activities of primary visual cortex (area 17) of cats are directly related with the perception of movement direction and line orientation. To date, there is not any report about the effect of BPA exposure on the visual receptive field properties on area 17 of adult cats. Since fluctuations of population have a great weight on processing of specific percepts and behavior, we analyzed changes occurring over the response fuctuations of population after BPA exposure.
METHODS: In the present study, BPA was administrated intravenously (i.v.) as saline solution (0.2mg/ml/h) for two hours. Using multiple-channel recording technique, we recorded responses of population and single neuron to different direction stimulation before and after BPA exposure.
RESULTS: The results showed that two key indexes of response fluctuations, noise correlation and signal correlation, were markedly upregulated after BPA exposure. We also found that BPA declined the direction discrimination capability of population after two hour exposure. These changes exhibited BPA exerted a negative effect on visual perception. To further study the alteration mechanism, response properties of single unit were examined based on orientation tuning. The results showed that BPA weakens the direction discrimination capacity and orientation selectivity capacity of the single neuron. Simultaneously, there is also a worse performance of information extraction capacity (signal to noise ratio) after dosing BPA.
CONCLUSIONS: Our present findings demonstrate that acute BPA exposure interferes the orientation perception in visual sensory system of adult cats due to decrease of orientation tuning in single neuron. Moreover, these results provide a new insight into BPA-induced brain function deterioration, revealing a more broad picture of its effect on cerebral cortex.