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Tonic adenosine A1 and A2A receptor activation is required for the excitatory action of VIP on synaptic transmission in the CA1 area of the hippocampus

dc.contributor.authorCunha-Reis, Diana
dc.contributor.authorFontinha, B. M.
dc.contributor.authorRibeiro, Joaquim A.
dc.contributor.authorSebastião, Ana M
dc.date.accessioned2013-04-12T15:13:11Z
dc.date.available2013-04-12T15:13:11Z
dc.date.issued2007
dc.description© 2006 Elsevier Ltdeng
dc.description.abstractAdenosine can regulate synaptic transmission through modulation of the action of other neurotransmitters. The influence of adenosine on VIP enhancement of synaptic transmission in hippocampal slices was investigated. Facilitation of fEPSP slope by 1 nM VIP (23.3 ± 1.3%) was turned into an inhibition (-12.1 ± 3.4%) when extracellular endogenous adenosine was removed using adenosine deaminase (ADA, 1 U/ml). Blockade of adenosine A1 receptors with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 nM) or of A2A receptors with ZM241385 (20 nM) attenuated the effect of VIP. When both DPCPX and ZM241385 were present the effect of VIP was abolished. In the presence of ADA, selective A1 receptor activation with N6-cyclopentyladenosine (CPA, 15 nM) or A2A receptor-activation with CGS21680 (10 nM) partially readmitted the excitatory effect of VIP on fEPSPs. In contrast, facilitation of PS amplitude by 1 nM VIP (19.1 ± 1.2%) was attenuated in the presence of ADA or DPCPX but was not changed by ZM241385. CPA, in the presence of ADA, fully restored the effect of VIP on PS amplitude. In conclusion, VIP facilitation of synaptic transmission to hippocampal pyramidal cell dendrites is dependent on both A1 and A2A receptor activation by endogenous adenosine. VIP effects on PS amplitude are only dependent on A1 adenosine receptor activation. This differential sensitivity to adenosine modulation might be due to the different VIP circuits contributing to VIP effects on pyramidal cell dendrites and pyramidal cell bodies.In contrast, facilitation of PS amplitude by 1 nM VIP (19.1 1.2%) was attenuated in the presence of ADA or DPCPX but was not changed by ZM241385. CPA, in the presence of ADA, fully restored the effect of VIP on PS amplitude. In conclusion, VIP facilitation of synaptic transmission to hippocampal pyramidal cell dendrites is dependent on both A1 and A2A receptor activation by endogenous adenosine. VIP effects on PS amplitude are only dependent on A1 adenosine receptor activation. This differential sensitivity to adenosine modulation might be due to the different VIP circuits contributing to VIP effects on pyramidal cell dendrites and pyramidal cell bodies. 1.2%) was attenuated in the presence of ADA or DPCPX but was not changed by ZM241385. CPA, in the presence of ADA, fully restored the effect of VIP on PS amplitude. In conclusion, VIP facilitation of synaptic transmission to hippocampal pyramidal cell dendrites is dependent on both A1 and A2A receptor activation by endogenous adenosine. VIP effects on PS amplitude are only dependent on A1 adenosine receptor activation. This differential sensitivity to adenosine modulation might be due to the different VIP circuits contributing to VIP effects on pyramidal cell dendrites and pyramidal cell bodies.eng
dc.description.sponsorshipFundacão para a Ciência e Tecnologia (FCT)por
dc.identifier.citationNeuropharmacology 52 (2007) 313-320por
dc.identifier.issn0028-3908
dc.identifier.urihttp://dx.doi.org/10.1016/j.neuropharm.2006.08.003
dc.identifier.urihttp://hdl.handle.net/10451/8275
dc.language.isoengpor
dc.peerreviewedyespor
dc.publisherElseviereng
dc.relation.publisherversionhttp://www.sciencedirect.com/eng
dc.subjectVIPeng
dc.subjectA2A adenosine receptorseng
dc.subjectA1 adenosine receptorseng
dc.subjectfEPSPseng
dc.subjectPSseng
dc.subjectHippocampuseng
dc.titleTonic adenosine A1 and A2A receptor activation is required for the excitatory action of VIP on synaptic transmission in the CA1 area of the hippocampuseng
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage320por
oaire.citation.startPage313por
oaire.citation.titleNeuropharmacologyeng
oaire.citation.volume52por
person.familyNameJerónimo da Cunha Reis
person.familyNameRibeiro
person.familyNameSebastião
person.givenNameDiana Lina
person.givenNameJoaquim
person.givenNameAna M
person.identifierF-1689-2011
person.identifier.ciencia-id1F1E-73C0-FD44
person.identifier.ciencia-id081F-2518-907F
person.identifier.ciencia-idF112-55E8-E37E
person.identifier.orcid0000-0002-0900-9306
person.identifier.orcid0000-0002-9330-3507
person.identifier.orcid0000-0001-9030-6115
person.identifier.scopus-author-id8571270200
person.identifier.scopus-author-id35498669400
person.identifier.scopus-author-id7004409879
rcaap.rightsrestrictedAccesspor
rcaap.typearticlepor
relation.isAuthorOfPublicationbd9c582c-30c6-4cf5-b91a-143562ce0931
relation.isAuthorOfPublication86da944c-5e6a-4ec5-a56e-4ed82ece7a17
relation.isAuthorOfPublication304abd7f-071b-4447-a8a3-4aa5f0547141
relation.isAuthorOfPublication.latestForDiscovery304abd7f-071b-4447-a8a3-4aa5f0547141

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