Bisphenol A exposure perturbs visual function of adult cats by remodeling the neuronal activity in the primary visual pathway.

摘要: Bisphenol A (BPA), a common environmental xenoestrogen, has been implicated in physiological and behavioral impairment, but the neuronal basis remains elusive. Although various synaptic mechanisms have shown to mediate BPA-induced brain deficits, there are almost no reports addressing its underlying at individual neuron level, particularly primary visual system. In present study, using multiple-channel recording technique, we recorded responses of single neurons system cats direction stimuli both before after BPA exposure. The results showed that orientation selectivity cortex (area 17, A17) was obviously decreased 2 h intravenous administration (0.2 mg/kg). Moreover, were worse performances information transmission A17 neurons, presenting markedly signal-to-noise ratio (SNR). To some extent, these functional decreases attributable altered inputs from lateral geniculate nucleus (LGN), which an increased spontaneous activity. Additionally, local injection (3.3 μg/ml) resulted obvious increase decrease activity, involving enhanced activity fast-spiking inhibitory interneurons. conclusion, our first demonstrate acute exposure can restrict perception cats, mainly depending on alteration LGN projection, not intercortical interaction. Importantly, BPA-induced-brain deficits might only be confined cortical level also occur as early subcortical level.