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dc.creatorOLGUÍN,PATRICIO
dc.creatorARMISEN,RICARDO
dc.creatorKUKULJAN,MANUEL
dc.date2006-01-01
dc.date.accessioned2019-05-02T21:21:33Z
dc.date.available2019-05-02T21:21:33Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000300010
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/81674
dc.descriptionThe electrophysiological properties of neurons are determined by the expression of defined complements of ion channels. Nonetheless, the regulation mechanisms of the expression of neuronal ion channels are poorly understood, due in part to the diversity of neuron subtypes. We explored the expression of voltage-gated currents of Xenopus primary spinal neurons unequivocally identified by means of single-cell RT-PCR. We found that identified spinal neurons exhibit heterogeneity in the temporal appearance of voltage-gated currents. Nevertheless, all neurons progress to similar functional phenotypes. A physiological feature is the onset and increase of the expression of sodium currents. To understand the mechanisms underlying this process, we studied the effect of a dominant negative form of the transcriptional silencer REST/NRSF and found that it associates to an increase in the density of sodium currents. This observation is compatible with a role of this factor in the regulation of gene expression in neurons. These experiments constitute a proof of principle for the feasibility of analyzing molecular mechanisms of the regulation of ion channel genes during early neuronal development and provide direct evidence of the role of REST/NRSF in the control of neuronal sodium channel expression.
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dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602006000300010
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.39 n.3 2006
dc.subjectexcitability
dc.subjectREST/NRSF
dc.subjectneuronal differentiation
dc.subjectsingle-cell RT-PCR transcription
dc.titleDevelopmental regulation of the expression of sodium currents in Xenopus primary neurons


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