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  3. FCEN - Facultad de Ciencias Exactas y Naturales. UBA
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dc.provenanceFacultad de Ciencias Exactas y Naturales de la UBA-
dc.contributor<div class="autor_fcen" id="6354">Pagani, M.R.</div>-
dc.contributorReisin, R.C.-
dc.contributor<div class="autor_fcen" id="8730">Uchitel, O.D.</div>-
dc.creator<div class="autor_fcen" id="6354">Pagani, M.R.</div>-
dc.creatorReisin, R.C.-
dc.creator<div class="autor_fcen" id="8730">Uchitel, O.D.</div>-
dc.date.accessioned2018-05-04T22:05:13Z-
dc.date.accessioned2018-05-28T15:48:27Z-
dc.date.available2018-05-04T22:05:13Z-
dc.date.available2018-05-28T15:48:27Z-
dc.date.issued2006-
dc.identifier.urihttp://10.0.0.11:8080/jspui/handle/bnmm/68490-
dc.descriptionSporadic amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects particularly motoneurons. Several pieces of evidence suggested the involvement of autoimmune mechanisms mediated by antibodies in ALS. However, the significance of those antibodies in the disease and the underlying mechanisms are unknown. Here we showed that IgG purified from a group of sporadic ALS patients, but not familial ALS patients, specifically interact with the presynaptic membrane of motoneurons through an antigen-antibody interaction and modulated synaptic transmission. Immunoreactivity against nerve terminals showed strong correlation with synaptic modulation ability. In addition, several controls have ruled out the possibility for this synaptic modulation to be mediated through proteases or nonspecific effects. Effective IgG potentiated both spontaneous and asynchronous transmitter release. Application of pharmacological inhibitors suggested that activation of this increased release required a nonconstitutive Ca2+ influx through N-type (Ca v2.2) channels and phospholipase C activity and that activation of IP3 and ryanodine receptors were necessary to both activate and sustain the increased release. Consistent with the notion that ALS is heterogeneous disorder, our results reveal that, in ∼50% of ALS patients, motor nerve terminals constitutes a target for autoimmune response. Copyright © 2006 Society for Neuroscience.-
dc.descriptionFil:Pagani, M.R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Uchitel, O.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.formatapplication/pdf-
dc.languageeng-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttp://creativecommons.org/licenses/by/2.5/ar-
dc.sourceJ. Neurosci. 2006;26(10):2661-2672-
dc.source.urihttp://digital.bl.fcen.uba.ar/Download/paper/paper_02706474_v26_n10_p2661_Pagani.pdf-
dc.subjectCalcium channels-
dc.subjectCalcium homeostasis alteration-
dc.subjectIP3R-
dc.subjectPhospholipase C-
dc.subjectRyR-
dc.subjectSignaling mechanisms-
dc.subjectcalcium-
dc.subjectcalcium channel N type-
dc.subjectcalcium ion-
dc.subjectimmunoglobulin G-
dc.subjectinositol trisphosphate-
dc.subjectneurotransmitter-
dc.subjectphospholipase C-
dc.subjectproteinase-
dc.subjectryanodine receptor-
dc.subjectadult-
dc.subjectaged-
dc.subjectamyotrophic lateral sclerosis-
dc.subjectanimal tissue-
dc.subjectantigen antibody reaction-
dc.subjectarticle-
dc.subjectautoimmunity-
dc.subjectcalcium signaling-
dc.subjectcalcium transport-
dc.subjectclinical article-
dc.subjectcontrolled study-
dc.subjectdegenerative disease-
dc.subjectenzyme activity-
dc.subjecthuman-
dc.subjectimmune response-
dc.subjectimmunoreactivity-
dc.subjectmale-
dc.subjectmotoneuron-
dc.subjectmouse-
dc.subjectnerve ending-
dc.subjectneuromodulation-
dc.subjectneurotransmitter release-
dc.subjectnonhuman-
dc.subjectpresynaptic membrane-
dc.subjectpriority journal-
dc.subjectreceptor upregulation-
dc.subjectsynaptic potential-
dc.subjectsynaptic transmission-
dc.subjectAdult-
dc.subjectAged-
dc.subjectAmyotrophic Lateral Sclerosis-
dc.subjectAnimals-
dc.subjectCalcium-
dc.subjectCalcium Channel Blockers-
dc.subjectCalcium Channels-
dc.subjectCalcium Channels, N-Type-
dc.subjectCalcium Signaling-
dc.subjectDose-Response Relationship, Radiation-
dc.subjectDrug Interactions-
dc.subjectElectric Stimulation-
dc.subjectEnzyme Inhibitors-
dc.subjectEvoked Potentials-
dc.subjectFemale-
dc.subjectHumans-
dc.subjectImmunoglobulin G-
dc.subjectImmunohistochemistry-
dc.subjectImmunoprecipitation-
dc.subjectInositol 1,4,5-Trisphosphate Receptors-
dc.subjectMale-
dc.subjectMice-
dc.subjectMiddle Aged-
dc.subjectMuscle Fibers-
dc.subjectNeuromuscular Junction-
dc.subjectNeurotransmitter Agents-
dc.subjectomega-Conotoxin GVIA-
dc.subjectPhospholipase C-
dc.subjectPresynaptic Terminals-
dc.subjectReceptors, Cytoplasmic and Nuclear-
dc.subjectRyanodine Receptor Calcium Release Channel-
dc.subjectStatistics-
dc.subjectSynaptic Transmission-
dc.subjectTime Factors-
dc.titleCalcium signaling pathways mediating synaptic potentiation triggered by amyotrophic lateral sclerosis IgG in motor nerve terminals-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:ar-repo/semantics/artículo-
dc.typeinfo:eu-repo/semantics/publishedVersion-
Aparece en las colecciones: FCEN - Facultad de Ciencias Exactas y Naturales. UBA

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