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Related Experiment Videos

Quinine blocks specific gap junction channel subtypes.

M Srinivas1, M G Hopperstad, D C Spray

  • 1Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA. msriniva@aecom.yu.edu

Proceedings of the National Academy of Sciences of the United States of America
|September 6, 2001
PubMed
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The antimalarial drug quinine selectively blocks specific gap junction channels, particularly those formed by connexin 36 (Cx36) and connexin 50 (Cx50). This action, occurring intracellularly, offers potential for targeted gap junction channel modulation.

Area of Science:

  • Pharmacology
  • Cell Biology
  • Neuroscience

Background:

  • Gap junctions mediate intercellular communication via connexin (Cx) channels.
  • Connexins play diverse roles in physiological and pathological processes.
  • Selective modulation of gap junction activity is therapeutically relevant.

Purpose of the Study:

  • To investigate the effect of the antimalarial drug quinine on various connexin-formed gap junctions.
  • To determine the selectivity and mechanism of quinine's action on gap junction channels.
  • To explore the potential of quinine as a tool for selective gap junction blockade.

Main Methods:

  • Transfected mammalian cell cultures expressing different connexins.
  • Electrophysiological recordings of junctional currents and single-channel activity.

Related Experiment Videos

  • pH manipulation and use of charged quinine derivatives to probe binding site.

    • Main Results:

    • Quinine reversibly blocked Cx36 and Cx50 gap junction currents with concentration dependence.
    • Quinine showed minimal to moderate effects on Cx26, Cx32, Cx40, Cx43, and Cx45 channels.
    • The binding site for quinine was determined to be intracellular, likely within the channel pore.
    • Quinine reduced channel open probability by inducing slow gating transitions.

    Conclusions:

    • Quinine exhibits connexin-selective inhibition of gap junction channels.
    • The intracellular binding site suggests a mechanism for pore blockade.
    • Quinine is a potential therapeutic agent for conditions involving Cx36 or Cx50 gap junctions.
    • Quinine derivatives may offer enhanced specificity for connexin-selective channel modulation.