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Inflammation in stroke: the role of cholinergic, purinergic and glutamatergic signaling

dc.contributor.authorMartín Muñoz, Abraham
dc.contributor.authorDomercq García, María ORCID
dc.contributor.authorMatute Almau, Carlos José
dc.date.accessioned2019-01-10T14:07:44Z
dc.date.available2019-01-10T14:07:44Z
dc.date.issued2018-05-04
dc.identifier.citationTherapeutic Advances in Neurological Disorders 11 : 1-14 (2018)es_ES
dc.identifier.issn1756-2856
dc.identifier.issn1756-2864
dc.identifier.urihttp://hdl.handle.net/10810/30731
dc.description.abstractThe inflammatory response is a major factor in stroke pathophysiology and contributes to secondary neuronal damage in both acute and chronic stages of the ischemic injury. Recent work in experimental cerebral ischemia has demonstrated the involvement of neurotransmitter signaling in the modulation of neuroinflammation. The present review discusses recent findings on the therapeutic potential and diagnostic perspectives of cholinergic, purinergic and glutamatergic receptors and transporters in experimental stroke. It provides evidence of the role of neurotransmission signaling as a promising inflammatory biomarker in stroke. Finally, recent molecular imaging studies using positron emission tomography of cholinergic receptors and glutamatergic transporters are outlined along with their potential as novel anti-inflammatory therapy to reduce the outcome of cerebral ischemia.es_ES
dc.description.sponsorshipWe acknowledge financial support by MINECO SAF2014-54070-JIN (A.M.) and SAF2016-75292-R (C.M.).es_ES
dc.language.isoenges_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/SAF2014-54070-JINes_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/SAF2016-75292-RRes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/es/*
dc.subjectcerebral ischemiaes_ES
dc.subjectcholinergices_ES
dc.subjectglutamatergices_ES
dc.subjectinflammationes_ES
dc.subjectpurinergices_ES
dc.subjectstroke:nicotinices_ES
dc.subjectacetylcholine-receptores_ES
dc.subjecttransient focal ischemiaes_ES
dc.subjectcerebral-ischemiaes_ES
dc.subjectsystem x(c)(-)es_ES
dc.subjectbrain ischemiaes_ES
dc.subjectcystine/glutamate antiporteres_ES
dc.subjectmicroglial cellses_ES
dc.subjectp2x(7) receptores_ES
dc.subjectantiinflammatory pathwayes_ES
dc.subjectactivated microgliaes_ES
dc.titleInflammation in stroke: the role of cholinergic, purinergic and glutamatergic signalinges_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.holderCreative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).es_ES
dc.rights.holderAtribución-NoComercial 3.0 España*
dc.relation.publisherversionhttps://journals.sagepub.com/doi/10.1177/1756286418774267es_ES
dc.identifier.doi10.1177/1756286418774267
dc.departamentoesNeurocienciases_ES
dc.departamentoeuNeurozientziakes_ES


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Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
Except where otherwise noted, this item's license is described as Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).