{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Lefton KB"],"funding":["NIDDK NIH HHS","NIMH NIH HHS","NINDS NIH HHS"],"pubmed_abstract":["Locus coeruleus (LC)-derived norepinephrine (NE) drives network and behavioral adaptations to environmental saliencies by reconfiguring circuit connectivity, but the underlying synapse-level mechanisms are elusive. Here, we show that NE remodeling of synaptic function is independent from its binding on neuronal receptors. Instead, astrocytic adrenergic receptors and Ca<sup>2+</sup> dynamics fully gate the effect of NE on synapses as the astrocyte-specific deletion of adrenergic receptors and three independent astrocyte-silencing approaches all render synapses insensitive to NE. Additionally, we find that NE suppression of synaptic strength results from an ATP-derived and adenosine A1 receptor-mediated control of presynaptic efficacy. An accompanying study from Chen et al. reveals the exist"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.05.21.595135"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11142048"],"repository":["biostudies-literature"],"pubmed_title":["Norepinephrine Signals Through Astrocytes To Modulate Synapses."],"pmcid":["PMC11142048"],"funding_grant_id":["R01 NS102272","R01 MH127163","R01 DK128475"],"pubmed_authors":["Walsh S","Samineni VK","Papouin T","Lefton KB","Yen A","Zhang Y","Okuda T","Dougherty JD","Manno R","Simpson PC","Wu Y","Dai Y"],"additional_accession":[]},"is_claimable":false,"name":"Norepinephrine Signals Through Astrocytes To Modulate Synapses.","description":"Locus coeruleus (LC)-derived norepinephrine (NE) drives network and behavioral adaptations to environmental saliencies by reconfiguring circuit connectivity, but the underlying synapse-level mechanisms are elusive. Here, we show that NE remodeling of synaptic function is independent from its binding on neuronal receptors. Instead, astrocytic adrenergic receptors and Ca<sup>2+</sup> dynamics fully gate the effect of NE on synapses as the astrocyte-specific deletion of adrenergic receptors and three independent astrocyte-silencing approaches all render synapses insensitive to NE. Additionally, we find that NE suppression of synaptic strength results from an ATP-derived and adenosine A1 receptor-mediated control of presynaptic efficacy. An accompanying study from Chen et al. reveals the exist","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-04-24T03:18:18.329Z","creation":"2026-04-24T03:09:46.776Z"},"accession":"S-EPMC11142048","cross_references":{"pubmed":["38826209"],"doi":["10.1101/2024.05.21.595135"]}}