Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A
Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A
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DOI：
10.1016/j.neuroscience.2008.12.028
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发表时间：
2009-03
期刊：
影响因子：
3.3
通讯作者：
Rong Zhou;Zhijun Zhang;Y. Zhu;Ling Chen;M. Sokabe
中科院分区：
文献类型：
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作者：
Rong Zhou;Zhijun Zhang;Y. Zhu;Ling Chen;M. Sokabe
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Prenatal and neonatal exposure to relatively low-dose bisphenol-A (BPA, 20 μg/kg/day) causes hyper-locomotion of male rat offspring. This research investigated the developmental pattern of activity-dependent synaptic plasticity in dorsolateral (DL) striatum, a cellular basis for motor controlling, in male rat offspring with hyper-locomotion. High frequency stimulation (four-pulse bursts at 100 Hz) was undertaken to induce long-term potentiation (LTP) and long-term depression (LTD) in corticostriatal synapse during postnatal day (PD) 10–32. Herein, we show that in control rats HFS induces LTP during PD12-14 and LTD during PD24-32. Strikingly, the prenatal and neonatal exposure to low-dose BPA resulted in delay of LTP induction during PD21-32, showing a reversal of LTD induction. In addition, in PD28 BPA-rats basal population spike amplitude was increased with reduction of paired-pulse facilitation (PPF) compared to the same age control rats. Acute application of the dopamine 1 receptor (D1R) antagonist SCH23390 in slices obtained from PD28 BPA-rats inhibited not only the PS-potentiation and PPF-induction but also the induction of LTP. Furthermore, the dopamine 2 receptor (D2R) agonist quinpirole recovered the LTD induction in PD28 BPA-rats, which was D1R-dependent and metabotropic glutamate receptor–dependent. In PD28 control rats, the blockade of D2R by l-sulpiride reversed the D1R- and mGluR-dependent LTD to short-term potentiation. Therefore, the findings provide functional evidence that prenatal and neonatal exposure to low-dose BPA causes deficits in development of LTP and LTD at DL-striatum via altering the function of dopaminergic receptors.