Abstract
Presently, it is thought that a non-voltage-gated current is responsible for activation-induced Ca2+ entry in nonelectrically excitable cells such as lymphocytes. However, it has also been proposed that the pathway instead involves a second messenger-regulated Ca2+ channel that is voltage operable, where "voltage operable" is defined as an intrinsic property of the channel protein(s) rather than a requirement of normal gating. To evaluate the contribution of these currents to activation-induced Ca2+ influx, each was examined with respect to its ability to account for Ca2+ influx as reported by Ca(2+)-sensitive dyes. We identified a set of reagents, nordihydroguaiaretic acid and various calmodulin inhibitors, that inhibits Ca2+ entry and blocks the voltage-operable current but leaves the non-voltage-gated current unaltered. Further-more, nordihydroguaiaretic acid inhibited Ca(2+)-dependent proliferation of mitogen-activated human peripheral blood mononuclear cells or Jurkat T cells and specifically blocked Ca(2+)-dependent interleukin 2 production by Jurkat T cells to a degree similar to the immunosuppressant drug cyclosporin A. We also identified compounds, amiloride and Mn2+, that block the non-voltage-gated current but have n...Continue Reading
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