Different Membrane Pathways Mediate Ca2+ Influx in Adrenal Chromaffin Cells Exposed to 150–400 ns Electric Pulses

Exposing adrenal chromaffin cells to 5 ns electric pulses (nsPEF) causes a rapid rise in intracellular Ca2+ () that is solely the result of Ca2+ influx through voltage-gated Ca2+ channels (VGCCs). This study explored the effect of longer duration nsPEF on . Single 150, 200, or 400 ns pulses at 3.1 kV/cm evoked rapid increases in , the magnitude of which increased linearly with pulse width and electric field amplitude. Recovery of to prestimulus levels was faster for 150 ns exposures. Regardless of pulse width, no rise in occurred in the absence of extracellular Ca2+, indicating that the source of Ca2+ was from outside the cell. Ca2+ responses evoked by a 150 ns pulse were inhibited to varying degrees by ω-agatoxin IVA, ω-conotoxin GVIA, nitrendipine or nimodipine, antagonists of P/Q-, N-, and L-type VGCCs, respectively, and by 67% when all four types of VGCCs were blocked simultaneously. The remaining Ca2+ influx insensitive to VGCC inhibitors was attributed to plasma membrane nanoporation, which comprised the -field sensitive component of the response. Both pathways of Ca2+ entry were inhibited by 200 μM Cd2+. These results demonstrate that, in excitable chromaffin cells, single 150–400 ns pulses increased the permeability of the plasma membrane to Ca2+ in addition to causing Ca2+ influx via VGCCs.

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