Olfactory neurons in bax knockout mice are protected from bulbectomy-induced apoptosis

Alan M. Robinson*, David B. Conley, Robert C. Kern

*Corresponding author for this work

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Surgical ablation of the olfactory bulb (bulbectomy) triggers a massive wave of apoptosis in mature olfactory sensory neurons within the olfactory epithelium. The aim of the current study was to determine if this process is dependent on expression of the pro-apoptotic protein Bax. Immunohistochemical detection of caspase-3 activation and olfactory epithelial thickness was used to demonstrate and quantify neuronal apoptosis in box knockout and wild type mice, following bulbectomy. Caspase-3 activation and epithelial thinning were both reduced in the box knockout mouse compared to the wild type mouse, at least up to 9 days post-bul-bectomy, indicating that apoptosis was inhibited not just delayed. This study demonstrates that Bax plays a major role in olfactory neuron apoptosis following surgical deafferentation.

Original languageEnglish (US)
Pages (from-to)1891-1894
Number of pages4
JournalNeuroreport
Volume14
Issue number15
DOIs
StatePublished - Oct 27 2003

Keywords

  • Bax
  • Bulbectomy
  • Caspase-3
  • Olfactory neurons

ASJC Scopus subject areas

  • Neuroscience(all)

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