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PMID:14561915
| Citation |
Robinson, AM, Conley, DB and Kern, RC (2003) Olfactory neurons in bax knockout mice are protected from bulbectomy-induced apoptosis. Neuroreport 14:1891-4 |
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| 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 bax knockout and wild type mice, following bulbectomy. Caspase-3 activation and epithelial thinning were both reduced in the bax knockout mouse compared to the wild type mouse, at least up to 9 days post-bulbectomy, indicating that apoptosis was inhibited not just delayed. This study demonstrates that Bax plays a major role in olfactory neuron apoptosis following surgical deafferentation. |
| Links |
PubMed Online version:10.1097/01.wnr.0000092464.31470.66 |
| Keywords |
Animals; Apoptosis/genetics; Apoptosis/physiology; Caspase 3; Caspases/metabolism; Denervation; Enzyme Activation/physiology; Epithelium/enzymology; Epithelium/physiology; Immunohistochemistry; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurons, Afferent/physiology; Olfactory Bulb/physiology; Olfactory Receptor Neurons/enzymology; Olfactory Receptor Neurons/physiology; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins c-bcl-2; bcl-2-Associated X Protein |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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