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Neuron–microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity

2022-01-21Journal article Open access
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dc.contributor.authorBravo, Joana
dc.contributor.authorRibeiro, Inês
dc.contributor.authorTerceiro, Ana Filipa
dc.contributor.authorAndrade, Elva B.
dc.contributor.authorPortugal, Camila Cabral
dc.contributor.authorLopes, Igor M.
dc.contributor.authorAzevedo, Maria M.
dc.contributor.authorSousa, Mafalda
dc.contributor.authorLopes, Cátia D. F.
dc.contributor.authorLobo, Andrea C.
dc.contributor.authorCanedo, Teresa
dc.contributor.authorRelvas, João Bettencourt
dc.contributor.authorSummavielle, Teresa
dc.date.accessioned2024-02-20T09:13:51Z
dc.date.available2024-02-20T09:13:51Z
dc.date.issued2022-01-21
dc.description.abstractExposure to methamphetamine (Meth) has been classically associated with damage to neuronal terminals. However, it is now becoming clear that addiction may also result from the interplay between glial cells and neurons. Recently, we demonstrated that binge Meth administration promotes microgliosis and microglia pro-inflammation via astrocytic glutamate release in a TNF/IP3R2-Ca2+-dependent manner. Here, we investigated the contribution of neuronal cells to this process. As the crosstalk between microglia and neurons may occur by contact-dependent and/or contact-independent mechanisms, we developed co-cultures of primary neurons and microglia in microfluidic devices to investigate how their interaction affects Meth-induced microglia activation. Our results show that neurons exposed to Meth do not activate microglia in a cell-autonomous way but require astrocyte mediation. Importantly, we found that neurons can partially prevent Meth-induced microglia activation via astrocytes, which seems to be achieved by increasing arginase 1 expression and strengthening the CD200/CD200r pathway. We also observed an increase in synaptic individual area, as determined by co-localization of pre- and post-synaptic markers. The present study provides evidence that contact-dependent mechanisms between neurons and microglia can attenuate pro-inflammatory events such as Meth-induced microglia activation.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBravo, J., Ribeiro, I., Terceiro, A. F., Andrade, E. B., Portugal, C. C., Lopes, I. M., Azevedo, M. M., Sousa, M., Lopes, C. D. F., Lobo, A. C., Canedo, T., Relvas, J. B., & Summavielle, T. (2022). Neuron–Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity. Cells, 11(3), Artigo 3. https://doi.org/10.3390/cells11030355pt_PT
dc.identifier.doi10.3390/cells11030355pt_PT
dc.identifier.eissn2073-4409
dc.identifier.urihttp://hdl.handle.net/10400.22/25038
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relationPOCI-01–0145-FEDER-022122pt_PT
dc.relation.publisherversionhttps://www.mdpi.com/2073-4409/11/3/355pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectMethamphetaminept_PT
dc.subjectNeuron-to-microgliapt_PT
dc.subjectNeuroprotectionpt_PT
dc.subjectContact-dependentpt_PT
dc.subjectCD200pt_PT
dc.subjectPSD95pt_PT
dc.titleNeuron–microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticitypt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage17pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleCellspt_PT
oaire.citation.volume11 (3)pt_PT
person.familyNameBravo
person.familyNameBonifácio Andrade
person.familyNameSummavielle
person.givenNameJoana
person.givenNameElva
person.givenNameTeresa
person.identifier677706
person.identifier.ciencia-idAA15-F362-062E
person.identifier.ciencia-id511C-11AA-7980
person.identifier.ciencia-idC41E-0816-5C85
person.identifier.orcid0000-0002-8403-7235
person.identifier.orcid0000-0002-1941-580X
person.identifier.orcid0000-0003-2548-6281
person.identifier.ridC-9776-2012
person.identifier.scopus-author-id6603092949
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication617f0f54-58dd-45b8-a90f-177187cd197e
relation.isAuthorOfPublicatione3b8883f-57b2-4b83-afa1-88e663ed8d1f
relation.isAuthorOfPublication207ee2de-85a0-4144-9e7e-b376c600e065
relation.isAuthorOfPublication.latestForDiscoverye3b8883f-57b2-4b83-afa1-88e663ed8d1f

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