Title : Targeting the inhibition of fatty acid amide hydrolase ameliorate the endocannabinoid-mediated synaptic dysfunction in a valproic acid-induced rat model of Autism.

Pub. Date : 2020 Jan 1

PMID : 31398381






3 Functional Relationships(s)
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1 Using an integrative approach combing electrophysiological and cellular mechanisms, the results showed that the impaired eCB-LTD, abnormal mGluR-mediated LTD (mGluR-LTD) and decreased removal of AMPAR subunits GluA1 and GluA2 were reversed by URB597 in the prefrontal cortex (PFC) of VPA-exposed offspring. cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus
2 Taken together, these results provide the first evidence that rescue of the ASD-like phenotype by URB597 is mediated by enhancing the mechanism of removal of AMPAR subunits GluA1/2 underlying AEA signaling in the PFC in a VPA-induced model of ASD. cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus
3 Taken together, these results provide the first evidence that rescue of the ASD-like phenotype by URB597 is mediated by enhancing the mechanism of removal of AMPAR subunits GluA1/2 underlying AEA signaling in the PFC in a VPA-induced model of ASD. cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus