Conditional ablation of mature olfactory sensory neurons mediated by diphtheria toxin receptor

Huaiyang Chen, Kenji Kohno, Qizhi Gong

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

The vertebrate olfactory epithelium provides an excellent model system to study the regulatory mechanisms of neurogenesis and neuronal differentiation due to its unique ability to generate new sensory neurons throughout life. The replacement of olfactory sensory neurons is stimulated when damage occurs in the olfactory epithelium. In this study, transgenic mice, with a transgene containing human diphtheria toxin receptor under the control of the olfactory marker protein promoter (OMP-DTR), were generated in which the mature olfactory sensory neurons could be specifically ablated when exposed to diphtheria toxin. Following diphtheria toxin induced neuronal ablation, we observed increased numbers of newly generated growth associated protein 43 (GAP43)-positive immature olfactory sensory neurons. OMP-positive neurons were continuously produced from the newly generated GAP43-positive cells. The expression of the signal transduction components adenylyl cyclase type III and the G-protein α subunit Gαolf was sensitive to diphtheria toxin exposure and their levels decreased dramatically preceding the disappearance of the OMP-positive sensory neurons. These data validate the hypothesis that OMP-DTR mice can be used as a tool to ablate the mature olfactory sensory neurons in a controlled fashion and to study the regulatory mechanisms of the neuronal replacement.

Original languageEnglish (US)
Pages (from-to)37-47
Number of pages11
JournalJournal of Neurocytology
Volume34
Issue number1-2
DOIs
StatePublished - Mar 2005

    Fingerprint

ASJC Scopus subject areas

  • Neuroscience(all)
  • Anatomy
  • Cell Biology
  • Histology

Cite this