Abstract
Kainate receptor activation affects GABAergic inhibition in the hippocampus by mechanisms that are thought to involve the GluR5 subunit. We report that disruption of the GluR5 subunit gene does not cause the loss of functional KARs in CA1 interneurons, nor does it prevent kainate-induced inhibition of evoked GABAergic synaptic transmission onto CA1 pyramidal cells. However, KAR function is abolished in mice lacking both GluR5 and GluR6 subunits, indicating that KARs in CA1 stratum radiatum interneurons are heteromeric receptors composed of both subunits. In addition, we show the presence of presynaptic KARs comprising the GluR6 but not the GluR5 subunit that modulate synaptic transmission between inhibitory interneurons. The existence of two separate populations of KARs in hippocampal interneurons adds to the complexity of KAR localization and function.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 475-484 |
| Number of pages | 10 |
| Journal | Neuron |
| Volume | 28 |
| Issue number | 2 |
| DOIs | |
| State | Published - 2000 |
Funding
This work was supported by grants and fellowships of the Centre National de la Recherche Scientifique, the Fondation pour la Recherche Médicale, and the Région Aquitaine to C. M., the Sweizerische Nationalfond and the Deutsche Forschungsgemeinschaft to A. S., and grants of the National Institute of Health and of the McKnight Foundation to S. F. H. The excellent technical assistance of Lora O'Leary and Cornelia Maron and of the animal research departments is gratefully acknowledged. We thank Alexandre Bouron, Ingrid Bureau, and Daniel Choquet for comments on this manuscript.
ASJC Scopus subject areas
- General Neuroscience