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Mutation Linked to Impaired Synaptic Transmission

Animal study supports idea that neuroligin-3 mutation contributes to autism development

THURSDAY, Sept. 6 (HealthDay News) -- A mutated protein -- the neuroligin-3 synaptic cell adhesion molecule -- increases inhibitory synaptic transmission in mice, which could have implications for how autism spectrum disorders develop in humans, according to the results of an animal study published in the Sept. 6 issue of Science.

Katsuhiko Tabuchi, M.D., of the University of Texas Southwestern Medical Center in Dallas, and colleagues studied the effects of introducing a mutation, the R451C-substitution in neuroligin-3, into mice.

The researchers found that mice with the mutation were less likely to interact with their cage companions, but had better spatial learning abilities than mice without the mutation. They also unexpectedly found that increased inhibitory synaptic transmission, without any apparent effect on excitatory synapses, accompanied these behavioral changes.

"Our data strongly support the notion that a change in the inhibitory/excitatory balance contributes to the pathogenesis of autism spectrum disorders," the authors conclude. "Such a change may alter oscillatory rhythms in brain. Given the relatively focused nature of behavioral abnormalities in the R451C KI mice and in some humans with idiopathic autism spectrum disorders, it is likely that this change is not global, but selectively affects only a subset of the many classes of inhibitory interneurons in the forebrain, a question that can now be addressed with the R451C KI mice."

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