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Collybistin is required for both the formation and maintenance of GABAergic postsynapses in the hippocampus


Papadopoulos, T; Eulenburg, V; Reddy-Alla, S; Mansuy, I M; Li, Y; Betz, H (2008). Collybistin is required for both the formation and maintenance of GABAergic postsynapses in the hippocampus. Molecular and Cellular Neuroscience, 39(2):161-169.

Abstract

Collybistin (Cb) is a brain-specific guanine nucleotide exchange factor, which interacts with the inhibitory receptor anchoring protein gephyrin. In the hippocampus of constitutively Cb-deficient adult mice, gephyrin and gephyrin-dependent GABAA receptors (GABAARs) are lost from postsynaptic sites. Here, we used a Cre–loxP system to inactivate the Cb gene in the forebrain at different developmental stages. Deletion of Cb during embryonic development prevented gephyrin clustering during synaptogenesis and caused an accumulation of gephyrin aggregates in the cell body of CA1 pyramidal neurons. Inactivation of the Cb gene during the third postnatal week resulted in a protracted loss of postsynaptic gephyrin clusters and the appearance of cytoplasmic gephyrin aggregates. These changes in gephyrin distribution were accompanied by a similar reduction in synaptically localized GABAAR γ2-subunit immunoreactivity. Our data show that Cb is required for both the initial localization and maintenance of gephyrin and gephyrin-dependent GABAARs at inhibitory postsynaptic membrane specializations in the hippocampus.

Collybistin (Cb) is a brain-specific guanine nucleotide exchange factor, which interacts with the inhibitory receptor anchoring protein gephyrin. In the hippocampus of constitutively Cb-deficient adult mice, gephyrin and gephyrin-dependent GABAA receptors (GABAARs) are lost from postsynaptic sites. Here, we used a Cre–loxP system to inactivate the Cb gene in the forebrain at different developmental stages. Deletion of Cb during embryonic development prevented gephyrin clustering during synaptogenesis and caused an accumulation of gephyrin aggregates in the cell body of CA1 pyramidal neurons. Inactivation of the Cb gene during the third postnatal week resulted in a protracted loss of postsynaptic gephyrin clusters and the appearance of cytoplasmic gephyrin aggregates. These changes in gephyrin distribution were accompanied by a similar reduction in synaptically localized GABAAR γ2-subunit immunoreactivity. Our data show that Cb is required for both the initial localization and maintenance of gephyrin and gephyrin-dependent GABAARs at inhibitory postsynaptic membrane specializations in the hippocampus.

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29 citations in Web of Science®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Brain Research Institute
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2008
Deposited On:29 Dec 2008 08:09
Last Modified:05 Apr 2016 12:34
Publisher:Elsevier
ISSN:1044-7431
Publisher DOI:10.1016/j.mcn.2008.06.006
PubMed ID:18625319
Permanent URL: http://doi.org/10.5167/uzh-5477

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