Translational control and autism-like behaviors

Christos G Gkogkas; Nahum Sonenberg

doi:10.4161/cl.24551

Translational control and autism-like behaviors

Christos G Gkogkas, Nahum Sonenberg

Deanery of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

Abstract

AUTISM SPECTRUM DISORDERS (ASD) CONSIST OF A SPECTRUM OF NEURODEVELOPMENTAL DISEASES WITH THREE SALIENT FEATURES: reduced social interactions, impaired communication and repetitive/stereotyped behaviors. In a recent study we found that increased eIF4E (eukaryotic initiation factor 4E)-dependent protein synthesis as a result of genetic deletion of Eif4ebp2 (eIF4E-binding protein 2) in mice, stimulates the production of neuroligins (Nlgns, synaptic cell-adhesion molecules important for synapse regulation) and engenders an imbalance of excitatory to inhibitory synaptic transmission (E/I) in CA1 pyramidal neurons. This imbalance is accompanied with deficits in social interaction, communication and repetitive/stereotyped behaviors in Eif4ebp2(-/-) mice. Using a compound that blocks cap-dependent translation or by knocking down Nlgn1, we restored the E/I balance and reversed the autism-like social deficits.

Original language	English
Pages (from-to)	e24551
Journal	Cellular logistics
Volume	3
Issue number	1
DOIs	https://doi.org/10.4161/cl.24551
Publication status	Published - 4 Apr 2013

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10.4161/cl.24551

Translational control and autism-like behaviors
Copyright © 2013 Landes Bioscience This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
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title = "Translational control and autism-like behaviors",

abstract = "AUTISM SPECTRUM DISORDERS (ASD) CONSIST OF A SPECTRUM OF NEURODEVELOPMENTAL DISEASES WITH THREE SALIENT FEATURES: reduced social interactions, impaired communication and repetitive/stereotyped behaviors. In a recent study we found that increased eIF4E (eukaryotic initiation factor 4E)-dependent protein synthesis as a result of genetic deletion of Eif4ebp2 (eIF4E-binding protein 2) in mice, stimulates the production of neuroligins (Nlgns, synaptic cell-adhesion molecules important for synapse regulation) and engenders an imbalance of excitatory to inhibitory synaptic transmission (E/I) in CA1 pyramidal neurons. This imbalance is accompanied with deficits in social interaction, communication and repetitive/stereotyped behaviors in Eif4ebp2(-/-) mice. Using a compound that blocks cap-dependent translation or by knocking down Nlgn1, we restored the E/I balance and reversed the autism-like social deficits.",

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Translational control and autism-like behaviors

Abstract

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