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dc.contributor.authorCrespo-Castrillo, Andrea
dc.contributor.authorPunzón, Eva
dc.contributor.authorPascual, Ricardo de
dc.contributor.authorMaroto, Marcos
dc.contributor.authorPadín, Juan Fernando
dc.contributor.authorGarcía-Álvarez, Isabel
dc.contributor.authorNanclares, Carmen
dc.contributor.authorRuiz-Pascual, Lucía
dc.contributor.authorGandía Juan, Luis 
dc.contributor.authorFernández-Mayoralas, Alfonso
dc.contributor.authorGarcía, Antonio G.
dc.contributor.otherUAM. Departamento de Farmacologíaes_ES
dc.date.accessioned2016-08-08T14:16:58Z
dc.date.available2016-08-08T14:16:58Z
dc.date.issued2015-12-01
dc.identifier.citationJournal of Neurochemistry 135.5 (2015): 880-896en_US
dc.identifier.issn0022-3042es_ES
dc.identifier.issn0022-3042es_ES
dc.identifier.urihttp://hdl.handle.net/10486/672389
dc.descriptionThis is the peer reviewed version of the following article: Novel synthetic sulfoglycolipid IG20 facilitates exocytosis in chromaffin cells through the regulation of sodium channels: Journal of Neurochemistre, 135.5 (2015), which has been published in final form at http://dx.doi.org/10.1111/jnc.13357en_US
dc.description.abstractIn searching for druggable synthetic lipids as potential modulators of synaptic transmission and plasticity, we synthesized sulfoglycolipid IG20 that stimulates neuritic outgrowth. Here we have explored its effects on ion channels and exocytosis in bovine chromaffin cells (BCCs). IG20 augmented the rate of basal catecholamine release. Such effect did not depend on Ca2+ mobilization from intracellular stores; rather, IG20-elicited secretion entirely dependent on Ca2+ entry through Lsubtype voltage-activated Ca2+ channels. Those channels were recruited by cell depolarization mediated by IG20 likely through its ability to enhance the recruitment of Na+ channels at more hyperpolarizing potentials. Confocal imaging with fluorescent derivative IG20-NBD revealed its rapid incorporation and confinement into the plasmalemma, supporting the idea that IG20 effects are exerted through a plasmalemmal-delimited mechanism. Thus, synthetic IG20 seems to mimic several physiological effects of endogenous lipids such as regulation of ion channels, Ca2+ signaling, and exocytosis. Therefore, sulfoglycolipid IG20 may become a pharmacological tool to investigate the role of the lipid environment on neuronal excitability, ion channels, neurotransmitter release, synaptic efficacy, and neuronal plasticity. It may also inspire the synthesis of druggable sulfoglycolipids aimed at increasing synaptic plasticity and efficacy in neurodegenerative diseases and traumatic brain – spinal cord injuryen_US
dc.description.sponsorshipThis work was supported by grants from Ministerio de Economía y Competitividad, Spain (MINECO, SAF-2013-44108-P to AGG and LG; and FIS-PI11/01436 to AFM), Fundación Eugenio Rodríguez Pascual (to LG). We thank the continued support of Fundación Teófilo Hernando, Madrid, Spainen_US
dc.format.extent24 pag.es_ES
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherJohn Wiley & Sons, Incen_US
dc.relation.ispartofJournal of Neurochemistryen_US
dc.rights© 2015 International Society for Neurochemistryen_US
dc.subject.otherCompound IG20en_US
dc.subject.otherExocytosisen_US
dc.subject.otherSodium channelen_US
dc.subject.otherCalcium channelen_US
dc.subject.otherSulfoglycolipiden_US
dc.subject.otherChromaffin cellen_US
dc.titleNovel synthetic sulfoglycolipid IG20 facilitates exocytosis in chromaffin cells through the regulation of sodium channelsen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.date.embargoend2016-12-01
dc.relation.publisherversionhttp://dx.doi.org/10.1111/jnc.13357en
dc.identifier.doi10.1111/jnc.13357es_ES
dc.identifier.publicationfirstpage880es_ES
dc.identifier.publicationissue5es_ES
dc.identifier.publicationlastpage896es_ES
dc.identifier.publicationvolume135es_ES
dc.relation.projectIDGobierno de España. SAF-2013-44108-Pes_ES
dc.relation.projectIDGobierno de España. FIS-PI11/01436es_ES
dc.type.versioninfo:eu-repo/semantics/acceptedVersionen
dc.rights.accessRightsopenAccessen
dc.facultadUAMFacultad de Medicina


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