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Beta N ‐acetylglucosaminyltransferase V (Mgat5) deficiency reduces the depression‐like phenotype in mice

Beta N ‐acetylglucosaminyltransferase V (Mgat5) deficiency reduces the depression‐like phenotype... The central nervous system (CNS) is rich in glycoconjugates, located on cell surface and in extracellular matrix. The products of Golgi UDP‐GlcNAc:N‐acetylglucosaminyltransferases (encoded by Mgat1, Mgat2, Mgat4 and Mgat5) act sequentially to generate the GlcNAc‐branched complex‐type N‐glycans on glycoprotein receptors. While elimination of all the branched N‐glycans in Mgat1−/− mouse embryos is lethal at neural tube fold stage, decreased branching is associated with late developmental defects similar to type 2 of congenital disorders of glycosylation, with developmental and psychomotor abnormalities. To study the role of complex‐type N‐glycans in brain function, we tested Mgat5−/− mice in a battery of neurological and behavioral tests. Despite the absence of tri‐ and tetra‐antennary products, Mgat5−/− mice were not different from their wild‐type littermates in physical and neurological assessments, anxiety level, startle reactivity and sensorimotor gating. However, they displayed a robust decrease in the immobility time in the forced swim test and the tail suspension test independent of locomotor activity, interpreted as a change in depression‐like behavior. This effect was accentuated after chronic mild stress. Comparable increase in plasma corticosterone of Mgat5+/+ and Mgat5−/− mice in response to acute stress shows an intact function of the hypothalamus–pituitary–adrenal axis. A change in social interactions was also observed. Our results indicate that Mgat5 modification of complex‐type N‐glycans on CNS glycoproteins is involved in the regulation of depression‐like behavior. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes, Brain and Behavior Wiley

Beta N ‐acetylglucosaminyltransferase V (Mgat5) deficiency reduces the depression‐like phenotype in mice

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References (62)

Publisher
Wiley
Copyright
© 2007 The Authors
ISSN
1601-1848
eISSN
1601-183X
DOI
10.1111/j.1601-183X.2007.00358.x
pmid
17883406
Publisher site
See Article on Publisher Site

Abstract

The central nervous system (CNS) is rich in glycoconjugates, located on cell surface and in extracellular matrix. The products of Golgi UDP‐GlcNAc:N‐acetylglucosaminyltransferases (encoded by Mgat1, Mgat2, Mgat4 and Mgat5) act sequentially to generate the GlcNAc‐branched complex‐type N‐glycans on glycoprotein receptors. While elimination of all the branched N‐glycans in Mgat1−/− mouse embryos is lethal at neural tube fold stage, decreased branching is associated with late developmental defects similar to type 2 of congenital disorders of glycosylation, with developmental and psychomotor abnormalities. To study the role of complex‐type N‐glycans in brain function, we tested Mgat5−/− mice in a battery of neurological and behavioral tests. Despite the absence of tri‐ and tetra‐antennary products, Mgat5−/− mice were not different from their wild‐type littermates in physical and neurological assessments, anxiety level, startle reactivity and sensorimotor gating. However, they displayed a robust decrease in the immobility time in the forced swim test and the tail suspension test independent of locomotor activity, interpreted as a change in depression‐like behavior. This effect was accentuated after chronic mild stress. Comparable increase in plasma corticosterone of Mgat5+/+ and Mgat5−/− mice in response to acute stress shows an intact function of the hypothalamus–pituitary–adrenal axis. A change in social interactions was also observed. Our results indicate that Mgat5 modification of complex‐type N‐glycans on CNS glycoproteins is involved in the regulation of depression‐like behavior.

Journal

Genes, Brain and BehaviorWiley

Published: Apr 1, 2008

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