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Isolating Nasal Olfactory Stem Cells from Rodents or Humans
Published on: August 22, 2011
Apoptosis in the aging olfactory epithelium
Alan M Robinson1, D B Conley, M J Shinners
1Department of Otolaryngology-Head and Neck Surgery, Northwestern University School of Medicine, Chicago, Illinois 60611, USA.
The Laryngoscope
|August 13, 2002
Summary
Aging increases pro-apoptotic gene expression in rat olfactory mucosa, mirroring deafferentation effects. This suggests age-related changes in olfactory receptor neurons contribute to declining smell sensation.
Area of Science:
- Neuroscience
- Cell Biology
- Gerontology
Background:
- Olfactory receptor neurons (ORNs) undergo baseline apoptosis, potentially due to environmental damage.
- Aging is associated with changes in gene expression within the olfactory mucosa.
- Understanding these changes is crucial for explaining age-related olfactory decline.
Purpose of the Study:
- To investigate age-related changes in apoptosis-regulating gene expression in rat olfactory mucosa.
- To compare these age-related changes with those induced by olfactory receptor neuron deafferentation.
Main Methods:
- Studied olfactory mucosae from young normal rats, old normal rats, and young rats post-olfactory bulb removal (deafferentation).
- Utilized Ribonuclease protection assays and histological analysis.
- Deafferentation was performed to induce controlled apoptosis and regeneration.
Main Results:
- Aged rats showed increased expression of pro-apoptotic genes (procaspase-3, bax) compared to young rats.
- Deafferented rats also exhibited increased expression of these pro-apoptotic genes.
- Gene expression changes in aged rats mimicked those seen after deafferentation.
Conclusions:
- Aging alters olfactory mucosa gene expression, favoring apoptosis and potentially increasing ORN fragility.
- These molecular changes may contribute to the age-related decline in olfactory sensation.
- The findings provide insights into the cellular mechanisms underlying olfactory aging.
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