Bisphenol A differently inhibits CaV3.1, Ca V3.2 and Ca V3.3 calcium channels.

Bisphenol A (BPA) is a widespread environmental contaminant detected in urine of 93 % of investigated US population. Recent epidemiological studies found correlation between BPA exposure and diseases including cardiovascular and neuronal disorders. BPA targets include hormone receptors and voltage-dependent ion channels.

NGF-induced neurite outgrowth in PC12 cells is independent of calcium entry through L-type calcium channels.

Neuronal growth factor (NGF) induces neurodifferentiation of PC12 cells into cholinergic neurons-like cells. It was shown that intracellular Ca2+ ions participate in regulation of the differentiation of PC12 cells. We tested whether L-type calcium channels contribute to Ca2+ entry which supports neurite outgrowth accompanying NGF-activated differentiation process.

T-type calcium channel blockers - new and notable.

Since cloning of the T-type or Ca(V)3.n calcium channel family in 1998-1999 much progress was made in investigation of their regulation. Most effective metal Ca(V)3 channel blockers are trivalent cations from lanthanide group together with transition metals La(3+) and Y(3+).

Haloperidol moderately inhibits cardiovascular L-type calcium current.

Effects of haloperidol on L-type CaV1.2 channel were studied. Calcium current was measured in whole cell patch-clamp using calcium as a charge carrier.

The effect of the outermost basic residues in the S4 segments of the Ca(V)3.1 T-type calcium channel on channel gating.

The contribution of voltage-sensing S4 segments in domains I to IV of the T-type Ca(V)3.1 calcium channel to channel gating was investigated by the replacement of the uppermost charged arginine residues by neutral cysteines. In each construct, either a single (R180C, R834C, R1379C or R1717C) or a double (two adjacent domains) mutation was introduced.

Effect of protein tyrosine kinase inhibitors on the current through the Ca(V)3.1 channel.

In the present study, we have investigated the effects of protein tyrosine kinase (PTK) inhibitors on the Ca(V)3.1 calcium channel stably transfected in HEK293 cells using the whole-cell configuration of the patch-clamp technique. We have tested two different tyrosine kinase inhibitors, genistein and tyrphostin AG213, and their inactive analogs, genistin and tyrphostin AG9.

Inorganic mercury and methylmercury inhibit the Cav3.1 channel expressed in human embryonic kidney 293 cells by different mechanisms.

Part of the neurotoxic effects of inorganic mercury (Hg(2+)) and methylmercury (MeHg) was attributed to their interaction with voltage-activated calcium channels. Effects of mercury on T-type calcium channels are controversial. Therefore, we investigated effects of Hg(2+) and MeHg on neuronal Ca(v)3.