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Toward a unifying model of malaria-induced channel activity

Guillaume Bouyer1, Stéphane Egée, Serge L Y Thomas

  • 1Laboratory of Cell Physiology of Erythrocytes, Centre National de la Recherche Scientifique, Université Pierre et Marie Curie, Unité Mixte de Recherche 7150, Station Biologique, B.P. 74, 29682 Roscoff Cedex, France.

Proceedings of the National Academy of Sciences of the United States of America
|June 20, 2007
PubMed

Insights

Malaria parasite Plasmodium falciparum infection dramatically increases red blood cell (RBC) membrane current. This current, carried by anion channels, is an enhanced form of channels present in uninfected RBCs, clarifying previous electrophysiological data.

Area of Science:

  • Electrophysiology
  • Malariology
  • Ion channel biophysics

Background:

  • Plasmodium falciparum infection of red blood cells (RBCs) induces a large membrane current.
  • This current was previously attributed to plasmodial surface anion channels (PSAC) observed under supraphysiological conditions.
  • Discrepancies exist in reported electrophysiological data regarding these parasite-induced channels.

Purpose of the Study:

  • To clarify electrophysiological data disparities concerning parasite-induced anion channels in infected RBCs.
  • To investigate the relationship between channels observed under physiological and supraphysiological conditions.
  • To identify the specific anion channels responsible for the increased membrane conductance.

Main Methods:

  • Single-channel recordings of infected and uninfected RBC membranes.
  • Electrophysiological measurements using both physiological (0.145 M Cl(-)) and supraphysiological (1.115 M Cl(-)) ion concentrations.
  • Inhibition studies using Zn(2+) to characterize channel function.

Main Results:

  • Plasmodial surface anion channels (PSAC) observed in supraphysiological conditions are the correlate of the small conductance anion channel (SCC) under physiological conditions.
  • Infected RBCs exhibit increased membrane conductance primarily due to an 18-pS inwardly rectifying anion channel (IRC) (80%) and SCC (20%) at physiological ion concentrations.
  • The IRC is functionally inhibited under supraphysiological conditions, leading to SCC (PSAC) dominating the conductance.

Conclusions:

  • The parasite-induced membrane current in Plasmodium falciparum-infected RBCs results from enhanced activity of endogenous anion channels, not solely parasite-derived channels.
  • The small conductance anion channel (SCC) is the physiological correlate of PSAC and likely a ClC-2 channel, inhibited by Zn(2+).
  • The inwardly rectifying anion channel (IRC) plays a significant role in the parasite-induced conductance under physiological conditions.

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