Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice

Christophe Mulle, Andreas Sailer, Isabel Pérez-Otaño, Heather Dickinson-Anson, Pablo E. Castillo, Ingrid Bureau, Cornelia Maron, Fred H. Gage, Jeffrey R. Mann, Bernhard Bettler and Stephen F. Heinemann ()
Additional contact information
Christophe Mulle: Molecular Neurobiology Laboratory
Andreas Sailer: Molecular Neurobiology Laboratory
Isabel Pérez-Otaño: Molecular Neurobiology Laboratory
Heather Dickinson-Anson: Laboratory of Genetics, The Salk Institute for Biological Studies
Pablo E. Castillo: Facultad de Medicina
Ingrid Bureau: UMR CNRS 5541, Université Victor Segalen-Bordeaux 2
Cornelia Maron: Molecular Neurobiology Laboratory
Fred H. Gage: Laboratory of Genetics, The Salk Institute for Biological Studies
Jeffrey R. Mann: Beckman Research Institute of the City of Hope
Bernhard Bettler: Molecular Neurobiology Laboratory
Stephen F. Heinemann: Molecular Neurobiology Laboratory

Nature, 1998, vol. 392, issue 6676, 601-605

Abstract: Abstract l-glutamate, the neurotransmitter of the majority of excitatory synapses in the brain, acts on three classes of ionotropic receptors: NMDA (N-methyl-d-aspartate), AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) and kainate receptors. Little is known about the physiological role of kainate receptors because in many experimental situations it is not possible to distinguish them from AMPA receptors1,2. Mice with disrupted kainate receptor genes enable the study of the specific role of kainate receptors in synaptic transmission as well as in the neurotoxic effects of kainate. We have now generated mutant mice lacking the kainate-receptor subunit GluR6. The hippocampal neurons in the CA3 region of these mutant mice are much less sensitive to kainate. In addition, a postsynaptic kainate current evoked in CA3 neurons by a train of stimulation of the mossy fibre system is absent in the mutant3,4. We find that GluR6-deficient mice are less susceptible to systemic administration of kainate, as judged by onset of seizures and by the activation of immediate early genes in the hippocampus. Our results indicate that kainate receptors containing the GluR6 subunit are important in synaptic transmission as well as in the epileptogenic effects of kainate.

Date: 1998
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/33408 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:392:y:1998:i:6676:d:10.1038_33408

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/33408

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().