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. 2016 Jul 3;10(4):253-5.
doi: 10.1080/19336950.2016.1172886. Epub 2016 Apr 5.

Electrophysiological evidences of interaction between calcium channels and PA of anthrax

Evgeny Kobrinsky  1 , Nikolai M Soldatov  1
Affiliations

Electrophysiological evidences of interaction between calcium channels and PA of anthrax

Evgeny Kobrinsky et al. Channels (Austin). .
No abstract available

Keywords: Cav1.2; anthrax; calcium channel; gabapentin; patch clamp; protective antigen.

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Figures

Figure 1.
Figure 1.
(A) Inhibition of calcium current by PA in Cos1 cells expressing human recombinant Cav1.2 composed of ECFPN-α1C,77/β3/α2δ-1 subunits. Peak calcium currents were elicited by a stepwise depolarization to +30 mV applied from the holding potential Vh=−90 mV before (left trace) and after (right trace) application of PA-U7 (500 ng/ml, closed circles; mean ± SEM, n = 3). A 90% inhibition occurred within 5–7 min at 20–22˚C. Under the same conditions, the inactive mutant of PA, PA-3M (500 ng/ml), did not induce notable inhibition of the Ca2+ current (open circles; n = 3). Slow linear decrease of the normalized current amplitude in control is due to rundown typically seen with the Cav1.2 calcium channels (see sample Ca2+ current trace, arrow). (B) Protective effect of gabapentin. When applied at 10 µM, gabapentin inhibited ˜60% of the calcium current in 10 min, the effect reaching apparent saturation (G). Subsequent application of PA (500 ng/ml) in the presence of 10 µM gabapentin (G+PA) for 10 min did not cause a significant additional inhibition of the calcium current amplitude, suggesting protection by gabapentin against the PA-dependent inhibition of the channel. Subsequent removal of gabapentin in the presence of PA (black bar PA) did not recover the PA-dependent block of the calcium current (dotted line) measured in the absence of gabapentin (white bar PA). Mean ± SEM; n = 5.
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