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Publication Detail
The role of pannexin hemichannels in the anoxic depolarization of hippocampal pyramidal cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Madry C, Haglerød C, Attwell D
  • Publication date:
    12/2010
  • Pagination:
    3755, 3763
  • Journal:
    Brain
  • Volume:
    133
  • Issue:
    Pt 12
  • Status:
    Published
  • Country:
    England
  • PII:
    awq284
  • Language:
    eng
  • Keywords:
    Adenosine Triphosphate, Aging, Animals, Brain Ischemia, CA1 Region, Hippocampal, Cell Hypoxia, Cell Membrane Permeability, Cell Separation, Coloring Agents, Connexins, Electrophysiological Phenomena, Extracellular Space, Glutamic Acid, Hippocampus, Ion Channels, Nerve Tissue Proteins, Patch-Clamp Techniques, Pyramidal Cells, Rats
Abstract
Neuronal gap junctional hemichannels, composed of pannexin-1 subunits, have been suggested to play a crucial role in epilepsy and brain ischaemia. After a few minutes of anoxia or ischaemia, neurons in brain slices show a rapid depolarization to ∼-20 mV, called the anoxic depolarization. Glutamate receptor blockers can prevent the anoxic depolarization, suggesting that it is produced by a cation influx through glutamate-gated channels. However, in isolated hippocampal pyramidal cells, simulated ischaemia evokes a large inward current and an increase in permeability to large molecules, mediated by the opening of pannexin-1 hemichannels. N-methyl-d-aspartate is also reported to open these hemichannels, suggesting that the activation of N-methyl-d-aspartate receptors, which occurs when glutamate is released in ischaemia, might cause the anoxic depolarization by evoking a secondary ion flux through pannexin-1 hemichannels. We tested the contribution of pannexin hemichannels to the anoxic depolarization in CA1 pyramidal cells in the more physiological environment of hippocampal slices. Three independent inhibitors of hemichannels-carbenoxolone, lanthanum and mefloquine-had no significant effect on the current generating the anoxic depolarization, while a cocktail of glutamate and gamma-aminobutyric acid class A receptor blockers abolished it. We conclude that pannexin hemichannels do not generate the large inward current that underlies the anoxic depolarization. Glutamate receptor channels remain the main candidate for generating the large inward current that produces the anoxic depolarization.
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