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GluK2-mediated excitability within the superficial layers of the entorhinal cortex

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Item Type:Article
Title:GluK2-mediated excitability within the superficial layers of the entorhinal cortex
Creators Name:Beed, P.S. and Salmen, B. and Schmitz, D.
Abstract:Recent analysis of genetically modified mice deficient in different kainate receptor (KAR) subunits have strongly pointed to a role of the GluK2 subunit, mediating the vulnerability of the brain towards seizures. Research concerning this issue has focused mainly on the hippocampus. However, several studies point to a potential role of other parts of the hippocampal formation, in particular the entorhinal cortex, in the development of epileptic seizures. There is extensive cell death after such seizures in layer III of the medial entorhinal cortex (LIII mEC), making this region of special interest for investigation into related pathological conditions. We therefore characterized KAR mediated currents in LIII mEC pyramidal neurons by several different approaches. Using patch-clamp technique, in combination with glutamate uncaging in horizontal brain slices, we show that LIII mEC neurons exhibit KAR currents. Use of genetically modified mice reveal that these currents are mediated by GluK2 containing KARs. The IV curve indicates the predominant presence of a Ca(2+) impermeable and edited form of the KAR. Finally, we show that GluK2 containing kainate receptors are essential for kainate-induced gamma oscillations within the entorhinal cortex.
Keywords:Anatomic Models, Biological Models, Electrophysiology, Entorhinal Cortex, Kainic Acid, Kainic Acid Receptors, Neurons, Patch-Clamp Techniques, Animals, Mice, Rats
Source:PLoS ONE
Publisher:Public Library of Science
Page Range:e5576
Date:18 May 2009
Additional Information:Erratum in: PLoS ONE. 2009;4(6).
Official Publication:https://doi.org/10.1371/journal.pone.0005576
PubMed:View item in PubMed

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