Abstract:
:Bisphenol-A (BPA), a toxic chemical from polycarbonate plastics, is known for behavioural and neural abnormalities. These neuro-behavioural changes reflect the changes in neural activity. However the effect of BPA on nerve action potential is not available. Therefore, present investigation was undertaken to study the effect of BPA on compound action potential (CAP) of frog sciatic nerve. Bundle containing small group of nerve fibres in a sciatic nerve was dissected and placed in a Perspex chamber perfused with Ringer solution. Suction electrodes were applied to the cut ends of the nerve for stimulating and recording purposes. The stimulation of one end (with supramaximal strength) produced CAP in the recording electrode. BPA (1-100 μM) decreased the amplitude and repolarization time of CAP in a concentration-dependent manner, without any alteration in latency, rise time and threshold. The decrease in amplitude was directly correlated with decrease in repolarization time (r=0.76). The BPA-induced decreases were absent in Ca(2+)-free medium or in presence of L-type Ca(2+)-channel antagonist (nifedipine/deltiazem). T and P type Ca(2+) channel antagonist (Ni(2+)) failed to block the BPA-induced responses. Pre-treatment with an Erα antagonist (tamoxifen) blocked the BPA-induced decrease in CAP parameters. These observations indicate that the BPA decreased the amplitude and repolarization time of CAP involving L-type Ca(2+)-channel dependent mechanisms. Further involvement of Erα in the modulation of Ca(2+) channels is a possibility.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Pandey AK,Deshpande SBdoi
10.1016/j.neulet.2012.04.044subject
Has Abstractpub_date
2012-05-31 00:00:00pages
128-32issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(12)00578-2journal_volume
517pub_type
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