Abstract
Intraerythrocyte survival of the malaria pathogen Plasmodium falciparumdepends on the induction of the new-permeability-pathways (NPPs) in the host cell membrane. NPPs are characterized as anion- and organic osmolyte-permeable channels which also exhibit a low but significant permeability for inorganic cations. To disclose the electrophyiologial properties of this infection-induced cation permeability whole-cell currents were recorded inPlasmodium falciparum-infected human erythrocytes (pRBC) using bath and pipette solutions with low Cl<sup>-</sup> concentrations. The data disclose a nonselective cation conductance (G<sub>cat</sub>) which activated upon removal of extracellular Cl<sup>-</sup>. Upon activation, G<sub>cat</sub> was 0.3 ± 0.05 nS (n=16) in control RBC and 2.0 ± 0.3 nS (n = 32) in pRBC indicating an induction of G<sub>cat</sub> during the infection. G<sub>cat</sub> of pRBC exibited a relative permselectivity for monovalent cations of Cs<sup>+</sup>ñK<sup>+</sup>>Na<sup>+</sup>>Li<sup>+</sup> (P<sub>Na</sub>/P<sub>K</sub> ñ 0.5) with a significant permeability for Ca<sup>2+</sup>. G<sub>cat</sub> of pRBC was inhibited by NPPs blockers (furosemide and NPPB) and cation channel blockers (amiloride, EIPA, GdCl<sub>3</sub>) with the highest sensitivity to EIPA (IC<sub>50</sub>ñ0.5µM). Most importantly, the blocker sensitivities differed between the infection-induced anion conductances and G<sub>cat</sub> suggesting that G<sub>cat</sub> and the anion conductances represent different channel proteins which in concert build up the NPPs.
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