Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributor.authorMartínez García, Albertcat
dc.contributor.authorAlcántara Horrillo, Soledadcat
dc.contributor.authorBorrell Franco, Víctorcat
dc.contributor.authorRío Fernández, José Antonio delcat
dc.contributor.authorBlasi Cabús, Joancat
dc.contributor.authorOtal Agudo, Raquelcat
dc.contributor.authorCampos Martínez, Narcisocat
dc.contributor.authorBoronat i Margosa, Albertcat
dc.contributor.authorBarbacid, Marianocat
dc.contributor.authorSilos-Santiago, Inmaculadacat
dc.contributor.authorSoriano García, Eduardocat
dc.description.abstractRecent studies have suggested a role for neurotrophins in the growth and refinement of neural connections, in dendritic growth, and in activity-dependent adult plasticity. To unravel the role of endogenous neurotrophins in the development of neural connections in the CNS, we studied the ontogeny of hippocampal afferents intrkB (¿/¿) and trkC (¿/¿) mice. Injections of lipophilic tracers in the entorhinal cortex and hippocampus of newborn mutant mice showed that the ingrowth of entorhinal and commissural/associational afferents to the hippocampus was not affected by these mutations. Similarly, injections of biocytin in postnatal mutant mice (P10¿P16) did not reveal major differences in the topographic patterns of hippocampal connections. In contrast, quantification of biocytin-filled axons showed that commissural and entorhinal afferents have a reduced number of axon collaterals (21¿49%) and decreased densities of axonal varicosities (8¿17%) in both trkB (¿/¿) and trkC (¿/¿) mice. In addition, electron microscopic analyses showed thattrkB (¿/¿) and trkC (¿/¿) mice have lower densities of synaptic contacts and important structural alterations of presynaptic boutons, such as decreased density of synaptic vesicles. Finally, immunocytochemical studies revealed a reduced expression of the synaptic-associated proteins responsible for synaptic vesicle exocytosis and neurotransmitter release (v-SNAREs and t-SNAREs), especially in trkB (¿/¿) mice. We conclude that neither trkB nor trkC genes are essential for the ingrowth or layer-specific targeting of hippocampal connections, although the lack of these receptors results in reduced axonal arborization and synaptic density, which indicates a role for TrkB and TrkC receptors in the developmental regulation of synaptic inputs in the CNS in vivo. The data also suggest that the genes encoding for synaptic proteins may be targets of TrkB and TrkC signaling pathways.eng
dc.format.extent15 p.-
dc.publisherSociety for Neuroscience-
dc.relation.isformatofReproducció del document publicat a:
dc.relation.ispartofThe Journal of Neuroscience, 1998, vol. 18, num. 18, p. 7336-7350-
dc.rights(c) Society for Neuroscience, 1998-
dc.sourceArticles publicats en revistes (Patologia i Terapèutica Experimental)-
dc.subject.classificationHipocamp (Cervell)cat
dc.subject.classificationProteïnes quinasescat
dc.subject.otherHippocampus (Brain)eng
dc.subject.otherProtein kinaseseng
dc.titleTrkB and TrkC signaling are required for maturation and synaptogenesis of hippocampal connectionseng
Appears in Collections:Articles publicats en revistes (Patologia i Terapèutica Experimental)

Files in This Item:
File Description SizeFormat 
148880.pdf1.04 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.