Wnt-5aoccludes Aβ oligomer-induced depression of glutamatergic transmission in hippocampal neurons

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dc.contributor.authorCerpa Nebott, Waldo Francisco
dc.contributor.authorFarías Galdames, Ginny Cheryl.
dc.contributor.authorGodoy Zeballos, Juan Alejandro
dc.contributor.authorInestrosa Cantín, Nibaldo
dc.contributor.authorFuenzalida, Marco.
dc.contributor.authorBonansco, Christian.
dc.date.accessioned2019-10-17T17:57:36Z
dc.date.available2019-10-17T17:57:36Z
dc.date.issued2010
dc.date.updated2019-10-14T18:52:18Z
dc.description.abstractAbstract Background Soluble amyloid-β (Aβ;) oligomers have been recognized to be early and key intermediates in Alzheimer's disease (AD)-related synaptic dysfunction. Aβ oligomers block hippocampal long-term potentiation (LTP) and impair rodent spatial memory. Wnt signaling plays an important role in neural development, including synaptic differentiation. Results We report here that the Wnt signaling activation prevents the synaptic damage triggered by Aβ oligomers. Electrophysiological analysis of Schaffer collaterals-CA1 glutamatergic synaptic transmission in hippocampal slices indicates that Wnt-5a increases the amplitude of field excitatory postsynaptic potentials (fEPSP) and both AMPA and NMDA components of the excitatory postsynaptic currents (EPSCs), without modifying the paired pulse facilitation (PPF). Conversely, in the presence of Aβ oligomers the fEPSP and EPSCs amplitude decreased without modification of the PPF, while the postsynaptic scaffold protein (PSD-95) decreased as well. Co-perfusion of hippocampal slices with Wnt-5a and Aβ oligomers occludes against the synaptic depression of EPSCs as well as the reduction of PSD-95 clusters induced by Aβ oligomers in neuronal cultures. Taken together these results indicate that Wnt-5a and Aβ oligomers inversely modulate postsynaptic components. Conclusion These results indicate that post-synaptic damage induced by Aβ oligomers in hippocampal neurons is prevented by non-canonical Wnt pathway activation.Abstract Background Soluble amyloid-β (Aβ;) oligomers have been recognized to be early and key intermediates in Alzheimer's disease (AD)-related synaptic dysfunction. Aβ oligomers block hippocampal long-term potentiation (LTP) and impair rodent spatial memory. Wnt signaling plays an important role in neural development, including synaptic differentiation. Results We report here that the Wnt signaling activation prevents the synaptic damage triggered by Aβ oligomers. Electrophysiological analysis of Schaffer collaterals-CA1 glutamatergic synaptic transmission in hippocampal slices indicates that Wnt-5a increases the amplitude of field excitatory postsynaptic potentials (fEPSP) and both AMPA and NMDA components of the excitatory postsynaptic currents (EPSCs), without modifying the paired pulse facilitation (PPF). Conversely, in the presence of Aβ oligomers the fEPSP and EPSCs amplitude decreased without modification of the PPF, while the postsynaptic scaffold protein (PSD-95) decreased as well. Co-perfusion of hippocampal slices with Wnt-5a and Aβ oligomers occludes against the synaptic depression of EPSCs as well as the reduction of PSD-95 clusters induced by Aβ oligomers in neuronal cultures. Taken together these results indicate that Wnt-5a and Aβ oligomers inversely modulate postsynaptic components. Conclusion These results indicate that post-synaptic damage induced by Aβ oligomers in hippocampal neurons is prevented by non-canonical Wnt pathway activation.
dc.fuente.origenBiomed Central
dc.identifier.citationMolecular Neurodegeneration. 2010 Jan 18;5(1):3
dc.identifier.doi10.1186/1750-1326-5-3
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/26805
dc.issue.numeroNo. 3
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final13
dc.pagina.inicio1
dc.revistaMolecular Neurodegenerationes_ES
dc.rightsacceso abierto
dc.rights.holderCerpa et al; licensee BioMed Central Ltd.
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.otherEnfermedad de Alzheimeres_ES
dc.subject.otherGlutamatoes_ES
dc.subject.otherCelulas nerviosases_ES
dc.subject.otherSistema nerviosoes_ES
dc.titleWnt-5aoccludes Aβ oligomer-induced depression of glutamatergic transmission in hippocampal neuronses_ES
dc.typeartículo
dc.volumenVol. 5
sipa.codpersvinculados16584
sipa.codpersvinculados102372
sipa.codpersvinculados99331
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