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

Alan M Robinson1, David B Conley, Robert C Kern

  • 1Department of Otolaryngology-Head and Neck Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. a-robinso2@northwestern.edu

Neuroreport
|October 17, 2003
PubMed

Insights

Bulbectomy causes olfactory neuron death, a process dependent on the Bax protein. Bax knockout mice showed reduced neuron apoptosis after surgery, indicating Bax

Area of Science:

  • Neuroscience
  • Cell Biology
  • Apoptosis Research

Background:

  • Surgical ablation of the olfactory bulb (bulbectomy) induces significant apoptosis in mature olfactory sensory neurons.
  • The pro-apoptotic protein Bax is a key regulator of programmed cell death.

Purpose of the Study:

  • To investigate the role of the pro-apoptotic protein Bax in olfactory neuron apoptosis following bulbectomy.
  • To determine if Bax expression is essential for the massive wave of apoptosis observed after olfactory bulb removal.

Main Methods:

  • Utilized immunohistochemical detection of caspase-3 activation to assess apoptosis.
  • Quantified olfactory epithelial thickness as a measure of neuronal loss.
  • Compared apoptosis levels in bax knockout mice versus wild-type mice post-bulbectomy.

Main Results:

  • Caspase-3 activation, a marker of apoptosis, was significantly reduced in bax knockout mice compared to wild-type mice.
  • Olfactory epithelial thinning, indicating neuronal loss, was also reduced in bax knockout mice.
  • These reductions were observed up to 9 days post-bulbectomy, suggesting inhibited, not merely delayed, apoptosis.

Conclusions:

  • Bax plays a critical role in mediating olfactory neuron apoptosis after surgical deafferentation (bulbectomy).
  • The absence of Bax significantly inhibits the apoptotic response of olfactory sensory neurons to bulbectomy.

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