Serveur d'exploration sur Heinrich Schütz

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Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice

Identifieur interne : 000599 ( Main/Exploration ); précédent : 000598; suivant : 000600

Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice

Auteurs : Theofilos Papadopoulos [Allemagne] ; Martin Korte [Allemagne] ; Volker Eulenburg [Allemagne] ; Hisahiko Kubota [Allemagne] ; Marina Retiounskaia [Allemagne] ; Robert J. Harvey [Royaume-Uni] ; Kirsten Harvey [Royaume-Uni] ; Gregory A. O'Sullivan [Allemagne] ; Bodo Laube [Allemagne] ; Swen Hülsmann [Allemagne] ; Jörg R P. Geiger [Allemagne] ; Heinrich Betz [Allemagne]

Source :

RBID : ISTEX:FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8

Abstract

Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.

Url:
DOI: 10.1038/sj.emboj.7601819


Affiliations:


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Le document en format XML

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