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Related Experiment Videos

The Lurcher mutation identifies delta 2 as an AMPA/kainate receptor-like channel that is potentiated by Ca(2+).

L P Wollmuth1, T Kuner, C Jatzke

  • 1Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794-5230, USA. lwollmuth@notes1.cc.sunysb.edu

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|August 10, 2000
PubMed
Summary

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The Lurcher mutation in delta 2 glutamate receptors causes neurodegeneration by constitutively activating these channels. These mutated channels mimic AMPA/kainate receptors, explaining cell death in Lurcher mice.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Ion Channel Physiology

Background:

  • Neurodegeneration in Lurcher (Lc) mice is linked to the constitutive activation of the delta 2 ionotropic glutamate receptor (GluR) subunit.
  • The natural ligands and channel properties of GluR-delta 2 have remained largely unknown.

Purpose of the Study:

  • To characterize the functional properties of homo-oligomeric GluR-delta 2 channels with the Lurcher mutation (GluR-delta 2(Lc)).
  • To investigate the role of the Q/R site in GluR-delta 2(Lc) channel function and Ca(2+) permeability.
  • To elucidate the potential mechanisms underlying neurodegeneration in Lurcher mice and cerebellar long-term depression.

Main Methods:

  • Expression of wild-type and mutated GluR-delta 2 channels in human embryonic kidney 293 cells.

Related Experiment Videos

  • Electrophysiological recordings to analyze current-voltage (I-V) relations, Ca(2+) permeability, and polyamine block.
  • Site-directed mutagenesis to alter the Q/R site in GluR-delta 2(Lc) channels.

    • Main Results:

    • GluR-delta 2(Lc) channels exhibited doubly rectifying I-V relations and Ca(2+) permeability (2-3%) similar to Ca(2+)-permeable AMPA/kainate channels.
    • Extracellular Ca(2+) potentiated GluR-delta 2(Lc) currents biphasically, with maximal effects at physiological concentrations.
    • Mutating the Q/R site (GluR-delta 2(Lc)(R)) abolished polyamine block and Ca(2+) permeability, but Ca(2+) potentiation remained.

    Conclusions:

    • GluR-delta 2(Lc) channels share functional similarities with AMPA/kainate receptor channels, particularly in their M2 and M3 segments.
    • Ca(2+) potentiation and permeability of GluR-delta 2(Lc) channels may explain cell death in Lurcher mice.
    • These findings offer insights into the physiological roles of GluR-delta 2 in cerebellar function, including long-term depression.