An absence of neuronal endocannabinoid signalling contributes to the behavioural and neurophysiological defects that are associated with fragile X syndrome - a common genetic cause of autism. The findings, reported in Nature Communications this week, provide new insights into the neurobiology of a disorder which is still poorly understood.
Fragile X syndrome - the most commonly inherited form of mental disability - is a major cause of autism spectrum disorder and is associated with a spectrum of mild-to-severe physical, intellectual and emotional symptoms. The main therapeutic strategies that are currently pursued by researchers involve enhancing glutamate-mediated synaptic plasticity. Glutamate signalling is known to be coupled to endocannabinoid signaling during normal functioning, however Oliver Manzoni and colleagues study a mouse model of fragile X syndrome and find that the endocannabinoid-glutamate signalling complex is uncoupled in these mice. They conclude that this uncoupling is responsible for the behavioural and neurophysiological effects associated with the disorder.
The authors suggest that their findings may provide the basis for creating novel therapeutic compounds.
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