Ítem
Acceso Abierto

Amyloid-? induces synaptic dysfunction through G protein-gated inwardly rectifying potassium channels in the fimbria-CA3 hippocampal synapse

Mostrar el registro sencillo de la publicación
dc.creatorNava Mesa, Mauricio Orlandospa
dc.creatorJiménez-Díaz, Lidiaspa
dc.creatorYajeya, Javierspa
dc.creatorNavarro-Lopez, Juan D.spa
dc.date.accessioned2020-08-19T14:40:11Z
dc.date.available2020-08-19T14:40:11Z
dc.date.created2013-07-25spa
dc.description.abstractLast evidences suggest that, in Alzheimer's disease (AD) early stage, Amyloid-? (A?) peptide induces an imbalance between excitatory and inhibitory neurotransmission systems resulting in the functional impairment of neural networks. Such alterations are particularly important in the septohippocampal system where learning and memory processes take place depending on accurate oscillatory activity tuned at fimbria-CA3 synapse. Here, the acute effects of A? on CA3 pyramidal neurons and their synaptic activation from septal part of the fimbria were studied in rats. A triphasic postsynaptic response defined by an excitatory potential (EPSP) followed by both early and late inhibitory potentials (IPSP) was evoked. The EPSP was glutamatergic acting on ionotropic receptors. The early IPSP was blocked by GABAA antagonists whereas the late IPSP was removed by GABAB antagonists. A? perfusion induced recorded cells to depolarize, increase their input resistance and decrease the late IPSP. A? action mechanism was localized at postsynaptic level and most likely linked to GABAB-related ion channels conductance decrease. In addition, it was found that the specific pharmacological modulation of the GABAB receptor effector, G-protein-coupled inward rectifier potassium (GirK) channels, mimicked all A? effects previously described.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.3389/fncel.2013.00117.
dc.identifier.issnISSN: 1662-5102
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/26751
dc.language.isoengspa
dc.publisherFrontiers Mediaspa
dc.relation.citationTitleFrontiers in Cellular Neuroscience
dc.relation.citationVolumeVol. 7
dc.relation.ispartofFrontiers in Cellular Neuroscience, ISSN: 1662-5102, Vol.7 (2015)spa
dc.relation.urihttps://www.frontiersin.org/articles/10.3389/fncel.2013.00117/fullspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.sourceFrontiers in Cellular Neurosciencespa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subject.keywordSeptohippocampal systemspa
dc.subject.keywordFimbria-CA3 synapsespa
dc.subject.keywordAmyloid-?25–35 peptidespa
dc.subject.keywordGABABspa
dc.subject.keywordGirK channelsspa
dc.subject.keywordAlzheimer's diseasespa
dc.subject.keywordBrain slicesspa
dc.subject.keywordIntracellular recordingsspa
dc.titleAmyloid-? induces synaptic dysfunction through G protein-gated inwardly rectifying potassium channels in the fimbria-CA3 hippocampal synapsespa
dc.title.TranslatedTitleEl amiloide-? induce una disfunción sináptica a través de los canales de potasio rectificadores hacia adentro activados por la proteína G en la sinapsis del hipocampo fimbria-CA3spa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
Archivos
Bloque original
Mostrando1 - 1 de 1
Miniatura
Nombre:
fncel-07-00117.pdf
Tamaño:
2.26 MB
Formato:
Adobe Portable Document Format
Descripción:
Descargar
Colecciones
Artículos