Abstract
Bisphenol A (BPA), an environmental xenoestrogen, has been reported to induce learning and memory impairments in rodent animals. However, effects of BPA exposure on synaptic plasticity and the underlying physiological mechanisms remain elusive. Our behavioral and electrophysiological analyses show that BPA obviously perturbs hippocampal spatial memory of juvenile Sprague–Dawley rats after four weeks exposure, with significantly impaired long‐term potentiation (LTP) in the hippocampus. These effects involve decreased spine density of pyramidal neurons, especially the apical dendritic spine. Further presynaptic findings show an overt inhibition of pulse‐paired facilitation during electrophysiological recording, which suggest the decrease of presynaptic transmitter release and is consistent with reduced production of presynaptic glutamate after BPA exposure. Meanwhile, LTP‐related glutamate receptors, NMDA receptor 2A (NR2A) and AMPA receptor 1 (GluR1), are significantly downregulated in BPA‐exposed rats. Excitatory postsynaptic currents (EPSCs) results also show that EPSCNMDA, but not EPSCAMPA, is declined by 40% compared to the baseline in BPA‐perfused brain slices. Taken together, these findings reveal that juvenile BPA exposure has negative effects on synaptic plasticity, which result from decreases in dendritic spine density and excitatory synaptic transmission. Importantly, this study also provides new insights into the dynamics of BPA‐induced memory deterioration during the whole life of rats.
Highlights
Bisphenol A (BPA), an environmental xenoestrogen, has been reported to so on.[1]
These findings reveal that juvenile BPA exposure periods of brain development) could induce memory deficits later in the life of rats, such as impaired spatial recognition memory in mid-adolescence,[6] and deficient spatial learning and memory in has negative effects on synaptic plasticity, which result from decreases in juvenile and adult.[7]
Combining behavioral assays and in vivo electrophysiology, the present study is the first to demonstrate that BPA exposure in juvenile rats deteriorated spatial memory and synaptic plasticity in the hippocampal CA1 areas
Summary
Escape latency of BPA-treated rats showed no significant difference with the control group, but an increasing trend (p > 0.05, Figure 2D). The current training and probe test results suggest that juvenile BPA exposure resulted in hippocampal-dependent spatial memory impairment without learning deficit. BPA-exposed rats had lower frequency of entry into the novel arm and higher frequency of entry into the home arm than the control group (p < 0.01, Figure 2I). These findings suggest the deficits of spatial memory for familiar environment in juvenile-BPA-exposed rats.
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