Antagonistic effects of TrkB and p75<SUP>NTR</SUP> on NMDA receptor currents in post-synaptic densities transplanted into <i>Xenopus</i> oocytes

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dc.contributor.authorSandoval, Mauricio
dc.contributor.authorSandoval, Rodrigo
dc.contributor.authorThomas, Ulrich
dc.contributor.authorSpilker, Christina
dc.contributor.authorSmalla, Karl-Heinz
dc.contributor.authorFalcon, Romina
dc.contributor.authorMarengo, Juan Jose
dc.contributor.authorCalderon, Rodrigo
dc.contributor.authorSaavedra, Veronica
dc.contributor.authorHeumann, Rolf
dc.contributor.authorBronfman, Francisca
dc.contributor.authorGarner, Craig C.
dc.contributor.authorGundelfinger, Eckart D.
dc.contributor.authorWyneken, Ursula
dc.date.accessioned2025-01-21T01:05:31Z
dc.date.available2025-01-21T01:05:31Z
dc.date.issued2007
dc.description.abstractBrain-derived neurotrophic factor (BDNF) and its receptor TrkB are essential regulators of synaptic function in the adult CNS. A TrkB-mediated effect at excitatory synapses is enhancement of NMDA receptor (NMDA-R)-mediated currents. Recently, opposing effects of TrkB and the pan-neurotrophin receptor p75(NTR) on long-term synaptic depression and long-term potentiation have been reported in the hippocampus. To further study the regulation of NMDA-Rs by neurotrophin receptors in their native protein environment, we micro-transplanted rat forebrain post-synaptic densities (PSDs) into Xenopus oocytes. One-minute incubations of oocytes with BDNF led to dual effects on NMDA-R currents: either TrkB-dependent potentiation or TrkB-independent inhibition were observed. Pro-nerve growth factor, a ligand for p75(NTR) but not for TrkB, produced a reversible, dose-dependent, TrkB-independent and p75(NTR)-dependent inhibition of NMDA-Rs. Fractionation experiments showed that p75(NTR) is highly enriched in the PSD protein fraction. Immunoprecipitation and pull-down experiments further revealed that p75(NTR) is a core component of the PSD, where it interacts with the PDZ3 domain of the scaffolding protein SAP90/PSD-95. Our data provide striking evidence for a rapid inhibitory effect of p75(NTR) on NMDA-R currents that antagonizes TrkB-mediated NMDA-R potentiation. These opposing mechanisms might be present in a large proportion of forebrain synapses and may contribute importantly to synaptic plasticity.
dc.fuente.origenWOS
dc.identifier.doi10.1111/j.1471-4159.2007.04519.x
dc.identifier.issn0022-3042
dc.identifier.urihttps://doi.org/10.1111/j.1471-4159.2007.04519.x
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/95944
dc.identifier.wosidWOS:000247135300021
dc.issue.numero6
dc.language.isoen
dc.pagina.final1684
dc.pagina.inicio1672
dc.revistaJournal of neurochemistry
dc.rightsacceso restringido
dc.subjectbrain-derived neurotrophic factor
dc.subjectneurotrophins
dc.subjectNMDA receptor
dc.subjectpost-synaptic density
dc.subjectsynapse
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleAntagonistic effects of TrkB and p75<SUP>NTR</SUP> on NMDA receptor currents in post-synaptic densities transplanted into <i>Xenopus</i> oocytes
dc.typeartículo
dc.volumen101
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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