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Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism

2012; American Association for the Advancement of Science; Volume: 338; Issue: 6103 Linguagem: Inglês

10.1126/science.1224159

1095-9203

Stéphane J. Baudouin, Julien Gaudias, Stefan Gerharz, Laetitia Hatstatt, Kuikui Zhou, Pradeep Punnakkal, Kenji F. Tanaka, Will Spooren, René Hen, Chris I. De Zeeuw, Kaspar E. Vogt, Peter Scheiffele,

Neuroscience and Neuropharmacology Research

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.