Bisphenol A depresses compound action potential of frog sciatic nerve in vitro involving Ca2+-dependent mechanisms

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 Ca2+-free medium or in presence of L-type Ca2+-channel antagonist (nifedipine/deltiazem). T and P type Ca2+ channel antagonist (Ni2+) 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 Ca2+-channel dependent mechanisms. Further involvement of Erα in the modulation of Ca2+ channels is a possibility.

► Effect of bisphenol A (BPA) was examined on frog sciatic nerve action potential.
► BPA decreased amplitude and repolarization time of compound action potential (CAP).
► BPA-induced decreases were absent in Ca2+-free medium.
► BPA-induced changes were blocked by L-type Ca2+ channel blockers and tamoxifen.
► CAP changes induced by BPA involve ERα and L-type Ca2+ channels.