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Chronic and acute adenosine A2A receptor blockade prevents long-term episodic memory disruption caused by acute cannabinoid CB1 receptor activation

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dc.contributor.authorMouro, Francisco
dc.contributor.authorBatalha, Vânia
dc.contributor.authorFerreira, Diana
dc.contributor.authorCoelho, Joana E
dc.contributor.authorBaqi, Younis
dc.contributor.authorMüller, Christa E.
dc.contributor.authorLopes, Luisa V.
dc.contributor.authorRibeiro, Joaquim A.
dc.contributor.authorSebastião, Ana M
dc.date.accessioned2022-06-08T15:43:53Z
dc.date.available2022-06-08T15:43:53Z
dc.date.issued2017
dc.description© 2017 Elsevier Ltd. All rights reserved.pt_PT
dc.description.abstractCannabinoid-mediated memory impairment is a concern in cannabinoid-based therapies. Caffeine exacerbates cannabinoid CB1 receptor (CB1R)-induced memory deficits through an adenosine A1 receptor-mediated mechanism. We now evaluated how chronic or acute blockade of adenosine A2A receptors (A2ARs) affects long-term episodic memory deficits induced by a single injection of a selective CB1R agonist. Long-term episodic memory was assessed by the novel object recognition (NOR) test. Mice received an intraperitoneal (i.p.) injection of the CB1/CB2 receptor agonist WIN 55,212-2 (1 mg/kg) immediately after the NOR training, being tested for novelty recognition 24 h later. Anxiety levels were assessed by the Elevated Plus Maze test, immediately after the NOR. Mice were also tested for exploratory behaviour at the Open Field. For chronic A2AR blockade, KW-6002 (istradefylline) (3 mg/kg/day) was administered orally for 30 days; acute blockade of A2ARs was assessed by i.p. injection of SCH 58261 (1 mg/kg) administered either together with WIN 55,212-2 or only 30 min before the NOR test phase. The involvement of CB1Rs was assessed by using the CB1R antagonist, AM251 (3 mg/kg, i.p.). WIN 55,212-2 caused a disruption in NOR, an action absent in mice also receiving AM251, KW-6002 or SCH 58261 during the encoding/consolidation phase; SCH 58251 was ineffective if present during retrieval only. No effects were detected in the Elevated Plus maze or Open Field Test. The finding that CB1R-mediated memory disruption is prevented by antagonism of adenosine A2ARs, highlights a possibility to prevent cognitive side effects when therapeutic application of CB1R drugs is desired.pt_PT
dc.description.sponsorshipWork supported by FCT (Fundação para a Ciência e Tecnologia, PTDC/DTP-FTO/3346/2014). FMM was in receipt of an FCT fellowship (SFRH/BD/89582/2012).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationNeuropharmacology. 2017 May 1;117:316-327pt_PT
dc.identifier.doi10.1016/j.neuropharm.2017.02.021pt_PT
dc.identifier.eissn1873-7064
dc.identifier.issn0028-3908
dc.identifier.urihttp://hdl.handle.net/10451/53348
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationSynaptic mechanisms involved in the brain cannabinoid actions and their modulation by adenosine receptors: implications for memory and mood control
dc.relationINTERACTION BETWEEN ADENOSINE A2A RECEPTORS AND CANNABINOID CB1 RECEPTORS AT THE HIPPOCAMPUS: CONSEQUENCES FOR PLASTICITY AND MEMORY
dc.relation.publisherversionhttps://www.sciencedirect.com/journal/neuropharmacologypt_PT
dc.subjectAdenosine A(2A) receptorpt_PT
dc.subjectCaffeinept_PT
dc.subjectCannabinoid receptor 1pt_PT
dc.subjectIstradefyllinept_PT
dc.subjectMemorypt_PT
dc.subjectNovel object recognitionpt_PT
dc.titleChronic and acute adenosine A2A receptor blockade prevents long-term episodic memory disruption caused by acute cannabinoid CB1 receptor activationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleSynaptic mechanisms involved in the brain cannabinoid actions and their modulation by adenosine receptors: implications for memory and mood control
oaire.awardTitleINTERACTION BETWEEN ADENOSINE A2A RECEPTORS AND CANNABINOID CB1 RECEPTORS AT THE HIPPOCAMPUS: CONSEQUENCES FOR PLASTICITY AND MEMORY
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FDTP-FTO%2F3346%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F89582%2F2012/PT
oaire.citation.endPage327pt_PT
oaire.citation.startPage316pt_PT
oaire.citation.titleNeuropharmacologypt_PT
oaire.citation.volume117pt_PT
oaire.fundingStream3599-PPCDT
person.familyNameMouro
person.familyNameBatalha
person.familyNameFerreira
person.familyNameCoelho
person.familyNameLopes
person.familyNameRibeiro
person.familyNameSebastião
person.givenNameFrancisco
person.givenNameVânia
person.givenNameDiana
person.givenNameJoana
person.givenNameLuisa
person.givenNameJoaquim
person.givenNameAna M
person.identifier548147
person.identifier149432
person.identifier.ciencia-idA915-3406-B4D3
person.identifier.ciencia-idB310-839B-564D
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person.identifier.orcid0000-0002-7141-8418
person.identifier.orcid0000-0001-6657-1111
person.identifier.orcid0000-0002-8072-613X
person.identifier.orcid0000-0002-3964-6197
person.identifier.orcid0000-0001-8367-3005
person.identifier.orcid0000-0002-9330-3507
person.identifier.orcid0000-0001-9030-6115
person.identifier.scopus-author-id7101840699
person.identifier.scopus-author-id7102509159
person.identifier.scopus-author-id35498669400
person.identifier.scopus-author-id7004409879
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT
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