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“Uncoupling Of The Endocannabinoid Signalling Complex In A Mouse Model Of Fragile X Syndrome.” Metadata:

  • Title: ➤  Uncoupling Of The Endocannabinoid Signalling Complex In A Mouse Model Of Fragile X Syndrome.
  • Authors: ➤  
  • Language: English

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  • Internet Archive ID: pubmed-PMC3657999

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This article is from <a href="//archive.org/search.php?query=journaltitle%3A%28Nature%20Communications%29" rel="nofollow">Nature Communications</a>, <a href="//archive.org/search.php?query=journaltitle%3A%28Nature%20Communications%29%20AND%20volume%3A%283%29" rel="nofollow">volume 3</a>.<h2>Abstract</h2>Fragile X syndrome, the most commonly known genetic cause of autism, is due to loss of the fragile X mental retardation protein, which regulates signal transduction at metabotropic glutamate receptor-5 in the brain. Fragile X mental retardation protein deletion in mice enhances metabotropic glutamate receptor-5-dependent long-term depression in the hippocampus and cerebellum. Here we show that a distinct type of metabotropic glutamate receptor-5-dependent long-term depression at excitatory synapses of the ventral striatum and prefrontal cortex, which is mediated by the endocannabinoid 2-arachidonoyl-sn-glycerol, is absent in fragile X mental retardation protein-null mice. In these mutants, the macromolecular complex that links metabotropic glutamate receptor-5 to the 2-arachidonoyl-sn-glycerol-producing enzyme, diacylglycerol lipase-α (endocannabinoid signalosome), is disrupted and metabotropic glutamate receptor-5-dependent 2-arachidonoyl-sn-glycerol formation is compromised. These changes are accompanied by impaired endocannabinoid-dependent long-term depression. Pharmacological enhancement of 2-arachidonoyl-sn-glycerol signalling normalizes this synaptic defect and corrects behavioural abnormalities in fragile X mental retardation protein-deficient mice. The results identify the endocannabinoid signalosome as a molecular substrate for fragile X syndrome, which might be targeted by therapy.

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