Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism

Author:

Baudouin Stéphane J.1,Gaudias Julien1,Gerharz Stefan1,Hatstatt Laetitia1,Zhou Kuikui2,Punnakkal Pradeep1,Tanaka Kenji F.34,Spooren Will5,Hen Rene3,De Zeeuw Chris I.26,Vogt Kaspar1,Scheiffele Peter1

Affiliation:

1. Biozentrum of the University of Basel, Basel, Switzerland.

2. Department of Neuroscience, Erasmus MC, Rotterdam, Netherlands.

3. Department of Neuroscience, Columbia University, New York, NY, USA.

4. Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan.

5. Hoffmann-La Roche, Basel, Switzerland.

6. Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, Netherlands.

Abstract

Reversing Autism in Mice Autism comprises a heterogeneous group of neurodevelopmental disorders characterized by defects in communication and social inter action. A group of nonsyndromic forms of autism is associated with mutations in the neuroligin genes, which encode postsynaptic adhesion molecules. Using a reversible knockout approach, Baudouin et al. (p. 128 , published online 13 September) investigated the in vivo functions of neuroligin-3 in the mouse cerebellum. Mutant mice showed a major defect in metabotropic glutamate receptor–dependent, long-term potentiation; disrupted heterosynaptic competition; and ectopic synapse formation in vivo. These synaptic defects could be rescued by reactivation of the neuroligin gene in the adult.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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