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TrkB receptor signaling and activity-dependent inhibitory synaptogenesis

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dc.contributor.authorSeil, F.J.es
dc.date.accessioned2011-06-08T09:02:56Z
dc.date.available2011-06-08T09:02:56Z
dc.date.issued2003
dc.description.abstractWhen mouse organotypic cerebellar cultures were exposed to anti-GABA agents that increased neuronal activity early in development, there was a doubling of the ratio of inhibitory axosomatic synapse profiles to Purkinje cell somatic profiles after two weeks in vitro, which correlated with a decrease in spontaneous cortical discharges. When similar cultures were maintained in medium with activity blocking agents, Purkinje cell axosomatic synapses were reduced to approximately half of control values and, after recovery from activity blockade, the cultures discharged hyperactively. By contrast, the full complement of excitatory cortical synapses developed in the absence of neuronal activity. These results support the concept that neuronal activity is necessary for the complete development of inhibitory circuitry. When cerebellar cultures were simultaneously exposed to activity blocking agents and to neurotrophins BDNF or NT-4, both of which bound to the TrkB receptor, the numbers of inhibitory Purkinje cell axosomatic synapses were similar to those of untreated control cultures, and control rates of spontaneous cortical discharges were recorded. The TrkC receptor ligand, NT-3, did not promote inhibitory synapse development in the absence of neuronal activity, and such cultures exhibited hyperactive cortical discharges. These results are consistent with a role for TrkB receptor ligands in activity-dependent inhibitory synaptogenesis. Subsequent exposure of cerebellar cultures to antibody to the extracellular domain of TrkB induced an increased development of Purkinje cell axosomatic synapses, while similar antibody activation of TrkC had no effect on inhibitory synaptogenesis. The promotion of inhibitory synapse development by specific antibody activation of TrkB supports the concept that signaling for activity-dependent inhibitory synaptogenesis is via the TrkB receptor.es
dc.formatapplication/pdfes
dc.format.extent12es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/21429
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectCerebellar cultureses
dc.subjectDevelopmentes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicinaes
dc.titleTrkB receptor signaling and activity-dependent inhibitory synaptogenesises
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.18, nº 2 (2003)