Researchers have elucidated a novel mechanism through which fragile x syndrome may contribute to behavioral symptoms of autism and identified a potential therapeutic target. Using a mouse model, they found that knocking- out the gene encoding fragile x intellectual disability protein caused the disruption of a special type of synaptic transmission that is dependent on an endocannabinoid factor. Crucially, pharmacological enhancement of this endocannabinoid restored some of the behavioral abnormalities of the knock-out mice, including impaired performance in a maze test.
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