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Adenosine receptors are the on‐and‐off switch of astrocytic cannabinoid type 1 (CB1) receptor effect upon synaptic plasticity in the medial prefrontal cortex

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dc.contributor.authorGonçalves-Ribeiro, Joana
dc.contributor.authorSavchak, Oksana K.
dc.contributor.authorPinto, Sara
dc.contributor.authorGomes, Joana I.
dc.contributor.authorRivas‐Santisteban, Rafael
dc.contributor.authorLillo, Alejandro
dc.contributor.authorSánchez Romero, Javier
dc.contributor.authorSebastião, Ana M
dc.contributor.authorNavarrete, Marta
dc.contributor.authorNavarro, Gemma
dc.contributor.authorFranco, Rafael
dc.contributor.authorVaz, Sandra H.
dc.date.accessioned2024-04-11T13:18:46Z
dc.date.available2024-04-11T13:18:46Z
dc.date.issued2024
dc.description© 2024 The Authors. GLIA published by Wiley Periodicals LLC. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.pt_PT
dc.description.abstractThe medial prefrontal cortex (mPFC) is involved in cognitive functions such as working memory. Astrocytic cannabinoid type 1 receptor (CB1R) induces cytosolic calcium (Ca2+) concentration changes with an impact on neuronal function. mPFC astrocytes also express adenosine A1 and A2A receptors (A1R, A2AR), being unknown the crosstalk between CB1R and adenosine receptors in these cells. We show here that a further level of regulation of astrocyte Ca2+ signaling occurs through CB1R-A2AR or CB1R-A1R heteromers that ultimately impact mPFC synaptic plasticity. CB1R-mediated Ca2+ transients increased and decreased when A1R and A2AR were activated, respectively, unveiling adenosine receptors as modulators of astrocytic CB1R. CB1R activation leads to an enhancement of long-term potentiation (LTP) in the mPFC, under the control of A1R but not of A2AR. Notably, in IP3R2KO mice, that do not show astrocytic Ca2+ level elevations, CB1R activation decreases LTP, which is not modified by A1R or A2AR. The present work suggests that CB1R has a homeostatic role on mPFC LTP, under the control of A1R, probably due to physical crosstalk between these receptors in astrocytes that ultimately alters CB1R Ca2+ signaling.pt_PT
dc.description.sponsorshipThis work was supported by the Fundaçao para a Ciência e para a Tecnologia (FCT) (grant PTDC/MED-FAR/30933/2017 to AMS, PD/BD/150342/2019 to JG-R and SFRH/BD/147277/2019 to SC-P), by the International Society for Neurochemistry (Carer Development Grant 2021 to SHV), the European Union (H2020-WIDESPREAD-05-2017-Twinning (EpiEpinet), grant agreement 952455, to AMS and SHV), the Spanish Ministry for Science, Innovation and Universities (MCIN/AEI/10.13039/501100011033) and the “ERDF A way of making Europe” (grant PID2021-122586NB-I00 to MN and PID2021-126600OB-I00 to RF), and the Fundación Tatiana Pérez de Guzmán el Bueno (PhD grant to JSR).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationGlia. 2024 Jun;72(6):1096-1116pt_PT
dc.identifier.doi10.1002/glia.24518pt_PT
dc.identifier.eissn1098-1136
dc.identifier.issn0894-1491
dc.identifier.urihttp://hdl.handle.net/10451/64145
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.relationIn the search of the synaptic mechanism operated by a novel selective antiepileptic drug
dc.relationAstrosomes: Artificial Astrocytes as a Novel Therapeutic to Amyotrophic Lateral Sclerosis ALS
dc.relationEpileptogenesis and Epilepsy Network: from genes, synapses and circuits to pave the way for novel drugs and strategies
dc.relation.publisherversionhttps://onlinelibrary.wiley.com/journal/10981136pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectCB1 receptorpt_PT
dc.subjectAdenosine receptorspt_PT
dc.subjectAstrogliapt_PT
dc.subjectmPFCpt_PT
dc.subjectSynaptic plasticitypt_PT
dc.titleAdenosine receptors are the on‐and‐off switch of astrocytic cannabinoid type 1 (CB1) receptor effect upon synaptic plasticity in the medial prefrontal cortexpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleIn the search of the synaptic mechanism operated by a novel selective antiepileptic drug
oaire.awardTitleAstrosomes: Artificial Astrocytes as a Novel Therapeutic to Amyotrophic Lateral Sclerosis ALS
oaire.awardTitleEpileptogenesis and Epilepsy Network: from genes, synapses and circuits to pave the way for novel drugs and strategies
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FMED-FAR%2F30933%2F2017/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//PD%2FBD%2F150342%2F2019/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F147277%2F2019/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/952455/EU
oaire.citation.endPage1116pt_PT
oaire.citation.issue6pt_PT
oaire.citation.startPage1096pt_PT
oaire.citation.titleGliapt_PT
oaire.citation.volume72pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamH2020
person.familyNameGonçalves Ribeiro
person.familyNameSavchak
person.familyNameCastro da Costa Pinto
person.familyNameGomes
person.familyNameSebastião
person.familyNameHenriques Vaz
person.givenNameJoana Filipa
person.givenNameOksana
person.givenNameSara Filipa
person.givenNameJoana I.
person.givenNameAna M
person.givenNameSandra Cristina
person.identifier695747
person.identifier694933
person.identifier.ciencia-id3018-692A-C792
person.identifier.ciencia-idB81D-4126-B667
person.identifier.ciencia-id7A17-D40A-D6F5
person.identifier.ciencia-idF112-55E8-E37E
person.identifier.ciencia-id0E1C-952D-61BE
person.identifier.orcid0000-0002-5194-6512
person.identifier.orcid0000-0003-0448-5343
person.identifier.orcid0000-0002-9785-8956
person.identifier.orcid0000-0001-7761-1983
person.identifier.orcid0000-0001-9030-6115
person.identifier.orcid0000-0003-4258-9397
person.identifier.scopus-author-id7004409879
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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