title: Deficits in development of synaptic plasticity in rat dorsal striatum following prenatal and neonatal exposure to low-dose bisphenol A.
abstract: Prenatal and neonatal exposure to relatively low-dose bisphenol-A (BPA, 20 microg/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.
authors.affiliation: Laboratory of Reproductive Medicine, Nanjing Medical University, Hanzhong Road 140, Jiangsu, China.
authors.forename: R
authors.initials: R
authors.lastname: Zhou
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Zhu
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: M
authors.initials: M
authors.lastname: Sokabe
authors.forename: L
authors.initials: L
authors.lastname: Chen
mesh_terms: D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001552:Benzazepines / Q000494:pharmacology; D001559:Benzhydryl Compounds; D003342:Corpus Striatum / Q000187:drug effects / Q000254:growth & development* / Q000473:pathology*; D018491:Dopamine Agonists / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects*; D010636:Phenols; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000473:pathology*; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000473:pathology*; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology; D000098826:Bisphenol A Compounds
chemical_list: D001552:Benzazepines; D001559:Benzhydryl Compounds; D018491:Dopamine Agonists; D018691:Excitatory Amino Acid Antagonists; D010636:Phenols; D011725:Pyridines; D014633:Valine; C534628:SCH 23390; C056639:2-amino-5-phosphopentanoic acid; C121465:6-methyl-2-(phenylethynyl)pyridine; C006780:bisphenol A; D000098826:Bisphenol A Compounds