Pflügers Archiv

, Volume 435, Issue 2, pp 310–319

Long-chain n-alkanols and arachidonic acid interfere with the Vm-sensitive gating mechanism of gap junction channels

  • R. Weingart
  • Feliksas F. Bukauskas
ORIGINAL ARTICLE

DOI: 10.1007/s004240050517

Cite this article as:
Weingart, R. & Bukauskas, F. Pflügers Arch (1997) 435: 310. doi:10.1007/s004240050517

Abstract

 Experiments were carried out on preformed cell pairs and induced cell pairs of an insect cell line (mosquito Aedes albopictus, clone C6/36). The coupling conductance, gj, was determined with the dual voltage-clamp method. Exposure of preformed cell pairs to lipophilic agents, such as long-chain n-alkanols (n-hexanol, n-heptanol, n-octanol, n-nonanol, n-decanol) or arachidonic acid, provoked a decrease in gj. Hyperpolarization of both cells led to a recovery of gj. Systematic studies revealed that this phenomenon is caused by a shift of the sigmoidal relationship gj(ss) = f(Vm) towards more negative values of Vm (where gj(ss) = conductance at steady-state; Vm = membrane potential). The shift was dose dependent, it developed with time and was reversible. The longer the hydrocarbon chain of n-alkanols, the lower was the concentration required to produce a given shift. Besides shifting the function gj(ss) = f(Vm), arachidonic acid decreased the maximal conductance, gj(max). Single-channel records gained from induced cell pairs revealed that the lipophilic agents interfere with the Vm-sensitive slow channel gating mechanism. Application provoked slow current transitions (transition time: 5–40 ms) between an open state of the channel (i.e. main state or residual state) and the closed state; subsequently, fast channel transitions (transition time: < 2 ms) involving the main state and the residual state ceased completely. Hyperpolarization of Vm or washout of the lipophilic agents gave rise to the inverse sequence of events. The single-channel conductances γj(main state) and γj(residual state) were not affected by n-heptanol. We conclude that long-chain n-alkanols and arachidonic acid interact with the Vm-sensitive gating mechanism.

Key words Insect gap junctionsLipophilic agentsChemical uncouplingSlow current transitionsVm-sensitive gatingn-AlkanolsArachidonic acid

Copyright information

© Springer-Verlag Berlin Heidelberg 1998

Authors and Affiliations

  • R. Weingart
    • 1
  • Feliksas F. Bukauskas
    • 1
  1. 1.Department of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, SwitzerlandCH
  2. 2.Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx NY 10461, USAUS