In vivo role of truncated trkB receptors during sensory ganglion neurogenesis

B. W. Luikart, S. Nef, T. Shipman, L. F. Parada

Research output: Contribution to journalArticle

49 Scopus citations

Abstract

The mammalian trkB locus undergoes alternative splicing to produce two different types of brain-derived neurotrophic factor receptors. The first type is the full-length receptor tyrosine kinase (TrkBTk+; the second type is a truncated receptor lacking the intracellular tyrosine kinase domain (TrkBTk-). To investigate the function of both types of TrkB receptor in vivo, we have generated knockout mice lacking all isoforms of the TrkB receptor (trkB-/-) and compared sensory neuron survival in these mice to that in the previously described TrkB kinase domain knockout mice (trkBk-/-). We observed that the presence of truncated TrkB receptors in trkBk-/- mice results in more severe sensory neuron losses. Increased neuron losses associated with the presence of truncated TrkB were most severe in regions where neuron survival is most dependent on brain-derived neurotrophic factor and neurotrophin-3. Our data suggest that truncated TrkB receptors negatively influence neuron survival by interfering with the function of catalytic TrkB receptors.

Original languageEnglish (US)
Pages (from-to)847-858
Number of pages12
JournalNeuroscience
Volume117
Issue number4
DOIs
StatePublished - Apr 10 2003

Keywords

  • BDNF
  • Neural development
  • Neuron survival
  • Neurotrophic factor

ASJC Scopus subject areas

  • Neuroscience(all)

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