Format

Send to

Choose Destination
See comment in PubMed Commons below
Nat Neurosci. 1998 Oct;1(6):470-8.

GluR5 kainate receptor activation in interneurons increases tonic inhibition of pyramidal cells.

Author information

1
Epilepsie et Ischémie Cérébrale, INSERM U29, Hôpital de Port Royal, Paris, France.

Abstract

We studied the modulation of GABAergic inhibition by glutamate and kainate acting on GluR5-containing kainate receptors in the CA1 hippocampal region. Glutamate, kainate or ATPA, a selective agonist of GluR5-containing receptors, generates an inward current in inhibitory interneurons and cause repetitive action potential firing. This results in a massive increase of tonic GABAergic inhibition in the somata and apical dendrites of pyramidal neurons. These effects are prevented by the GluR5 antagonist LY 293558. Electrical stimulation of excitatory afferents generates kainate receptor-mediated excitatory postsynaptic currents (EPSCs) and action potentials in identified interneurons that project to the dendrites and somata of pyramidal neurons. Therefore glutamate acting on kainate receptors containing the GluR5 subunit may provide a protective mechanism against hyperexcitability.

Comment in

PMID:
10196544
DOI:
10.1038/2185
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Support Center