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Endogenous VIP VPAC1 receptor activation modulates hippocampal theta burst induced LTP: transduction pathways and GABAergic mechanisms

2022Journal article Open access
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dc.contributor.authorCaulino-Rocha, Ana
dc.contributor.authorRodrigues, Nádia Carolina
dc.contributor.authorRibeiro, Joaquim A.
dc.contributor.authorCunha-Reis, Diana
dc.date.accessioned2022-12-06T15:37:26Z
dc.date.available2022-12-06T15:37:26Z
dc.date.issued2022
dc.description© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).pt_PT
dc.description.abstractVasoactive intestinal peptide (VIP), acting on both VPAC1 and VPAC2 receptors, is a key modulator of hippocampal synaptic transmission, pyramidal cell excitability and long-term depression (LTD), exerting its effects partly through modulation GABAergic disinhibitory circuits. Yet, the role of endogenous VIP and its receptors in modulation of hippocampal LTP and the involvement of disinhibition in this modulation have scarcely been investigated. We studied the modulation of CA1 LTP induced by TBS via endogenous VIP release in hippocampal slices from young-adult Wistar rats using selective VPAC1 and VPAC2 receptor antagonists, evaluating its consequence for the phosphorylation of CamKII, GluA1 AMPA receptor subunits and Kv4.2 potassium channels in total hippocampal membranes obtained from TBS stimulated slices. Endogenous VIP, acting on VPAC1 (but not VPAC2) receptors, inhibited CA1 hippocampal LTP induced by TBS in young adult Wistar rats and this effect was dependent on GABAergic transmission and relied on the integrity of NMDA and CaMKII-dependent LTP expression mechanisms but not on PKA and PKC activity. Furthermore, it regulated the autophosphorylation of CaMKII and the expression and Ser438 phosphorylation of Kv4.2 potassium channels responsible for the A-current while inhibiting phosphorylation of Kv4.2 on Thr607. Altogether, this suggests that endogenous VIP controls the expression of hippocampal CA1 LTP by regulating disinhibition through activation of VPAC1 receptors in interneurons. This may impact the autophosphorylation of CaMKII during LTP, as well as the expression and phosphorylation of Kv4.2 K+ channels at hippocampal pyramidal cell dendrites.pt_PT
dc.description.sponsorshipThis work was supported national and international funding managed by Fundação para a Ciência e a Tecnologia (FCT, IP), Portugal. Grants: FCT UIDB/04046/2020 and UIDP/04046/2020 to BioISI, PTDC/SAU-NEU/103639/2008; and FCT/POCTI (PTDC/SAU-PUB/28311/2017) EPIRaft grant to DCR. Fellowships: SFRH/BPD/81358/2011 to DCR and Researcher contract: Norma Transitória—DL57/2016/CP1479/CT0044 to DCR.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBiology (Basel). 2022 Apr 20;11(5):627pt_PT
dc.identifier.doi10.3390/biology11050627pt_PT
dc.identifier.eissn2079-7737
dc.identifier.urihttp://hdl.handle.net/10451/55361
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relationDL57/2016/CP1479/CT0044pt_PT
dc.relationBiosystems and Integrative Sciences Institute
dc.relationBiosystems and Integrative Sciences Institute
dc.relationContribution of neuronal membrane and lipid raft remodelling to the pathophysiology of mesial temporal lobe epilepsy (MTLE): insight into the beneficial effects of the ketogenic diet therapy.
dc.relationEVALUATING THERAPEUTIC OPPORTUNITIES FOR PREVENTING EPILEPTOGENESIS, COGNITIVE DECLINE AND SUDDEN DEATH IN EPILEPSY
dc.relation.publisherversionhttps://www.mdpi.com/journal/biologypt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectKv4.2pt_PT
dc.subjectLTPpt_PT
dc.subjectVIPpt_PT
dc.subjectVPAC1 receptorspt_PT
dc.subjectVPAC2 receptorspt_PT
dc.subjectHippocampuspt_PT
dc.subjectInterneuronspt_PT
dc.titleEndogenous VIP VPAC1 receptor activation modulates hippocampal theta burst induced LTP: transduction pathways and GABAergic mechanismspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleBiosystems and Integrative Sciences Institute
oaire.awardTitleBiosystems and Integrative Sciences Institute
oaire.awardTitleContribution of neuronal membrane and lipid raft remodelling to the pathophysiology of mesial temporal lobe epilepsy (MTLE): insight into the beneficial effects of the ketogenic diet therapy.
oaire.awardTitleEVALUATING THERAPEUTIC OPPORTUNITIES FOR PREVENTING EPILEPTOGENESIS, COGNITIVE DECLINE AND SUDDEN DEATH IN EPILEPSY
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDB%2F04046%2F2020/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDP%2F04046%2F2020/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-NEU%2F103639%2F2008/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FSAU-PUB%2F28311%2F2017/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/OE/SFRH%2FBPD%2F81358%2F2011/PT
oaire.citation.issue5pt_PT
oaire.citation.titleBiologypt_PT
oaire.citation.volume11pt_PT
oaire.fundingStream6817 - DCRRNI ID
oaire.fundingStream6817 - DCRRNI ID
oaire.fundingStream3599-PPCDT
oaire.fundingStream9471 - RIDTI
oaire.fundingStreamOE
person.familyNameVeiga Caulino Rocha
person.familyNameRibeiro
person.familyNameJerónimo da Cunha Reis
person.givenNameAna
person.givenNameJoaquim
person.givenNameDiana Lina
person.identifierhttps://scholar.google.com/citations?hl=pt-PT&user=xHrOBNgAAAAJ
person.identifierF-1689-2011
person.identifier.ciencia-id0916-863C-8374
person.identifier.ciencia-id081F-2518-907F
person.identifier.ciencia-id1F1E-73C0-FD44
person.identifier.orcid0000-0002-4051-5952
person.identifier.orcid0000-0002-9330-3507
person.identifier.orcid0000-0002-0900-9306
person.identifier.scopus-author-id57217380631
person.identifier.scopus-author-id35498669400
person.identifier.scopus-author-id8571270200
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/10.13039/501100001871
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
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
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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