{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nagai J"],"funding":["NICHD NIH HHS","NIDA NIH HHS","NHLBI NIH HHS","Medical Research Council","NINDS NIH HHS"],"pagination":["2256-2274.e9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8418870"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["109(14)"],"pubmed_abstract":["Astrocytes respond to neurotransmitters and neuromodulators using G-protein-coupled receptors (GPCRs) to mediate physiological responses. Despite their importance, there has been no method to genetically, specifically, and effectively attenuate astrocyte G<sub>q</sub> GPCR pathways to explore consequences of this prevalent signaling mechanism in vivo. We report a 122-residue inhibitory peptide from β-adrenergic receptor kinase 1 (iβARK; and inactive D110A control) to attenuate astrocyte G<sub>q</sub> GPCR signaling. iβARK significantly attenuated G<sub>q</sub> GPCR Ca<sup>2+</sup> signaling in brain slices and, in vivo, altered behavioral responses, spared other GPCR responses, and did not alter astrocyte spontaneous Ca<sup>2+</sup> signals, morphology, electrophysiological properties, or "],"journal":["Neuron"],"pubmed_title":["Specific and behaviorally consequential astrocyte G<sub>q</sub> GPCR signaling attenuation in vivo with iβARK."],"pmcid":["PMC8418870"],"funding_grant_id":["R35 NS111583","R01 DA047444","R00 HL132882","UKDRI-4007","U54 HD087101","K99 HL132882","P30 NS062691","R01 NS116589"],"pubmed_authors":["Gangwani MR","Gradinaru V","Nagai J","Schumacher SM","Diaz-Castro B","Bellafard A","Qu Z","Khakh BS","Golshani P","Coppola G","Yu X","Ollivier M"],"additional_accession":[]},"is_claimable":false,"name":"Specific and behaviorally consequential astrocyte G<sub>q</sub> GPCR signaling attenuation in vivo with iβARK.","description":"Astrocytes respond to neurotransmitters and neuromodulators using G-protein-coupled receptors (GPCRs) to mediate physiological responses. Despite their importance, there has been no method to genetically, specifically, and effectively attenuate astrocyte G<sub>q</sub> GPCR pathways to explore consequences of this prevalent signaling mechanism in vivo. We report a 122-residue inhibitory peptide from β-adrenergic receptor kinase 1 (iβARK; and inactive D110A control) to attenuate astrocyte G<sub>q</sub> GPCR signaling. iβARK significantly attenuated G<sub>q</sub> GPCR Ca<sup>2+</sup> signaling in brain slices and, in vivo, altered behavioral responses, spared other GPCR responses, and did not alter astrocyte spontaneous Ca<sup>2+</sup> signals, morphology, electrophysiological properties, or ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jul","modification":"2026-05-09T03:09:25.177Z","creation":"2025-04-05T14:08:24.204Z"},"accession":"S-EPMC8418870","cross_references":{"pubmed":["34139149"],"doi":["10.1016/j.neuron.2021.05.023"]}}