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Correspondence. Localised degeneration occurs in aged mouse olfactory epithelium

Published online by Cambridge University Press:  01 July 1997

L. J. BRECKENRIDGE
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
J. CAMERON
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
N. PURI
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
O. REID
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
J. MCGADEY
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
R. A. SMITH
Affiliation:
Laboratory of Human Anatomy, Institute of Biomedical & Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
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Abstract

Olfactory neuroepithelium of adult vertebrates retains a population of basal stem cells capable, throughout life, of dividing and differentiating into mature olfactory receptor neurons (see Farbman, 1994). The rate of turnover of olfactory receptor neurons is influenced, in part, by environmental conditions (Hinds et al. 1984). The olfactory system is known, however, to undergo a general decline in function with age. Age-related changes have been described in the rat olfactory bulb, with a decline in size in later life (Hinds & McNelly, 1981). However, this was thought to be secondary to changes within the olfactory epithelium as changes in the number of olfactory receptor neurons directly influence the size of the olfactory bulb. Thus the primary deficit in declining olfactory function may reside in the olfactory epithelium. Studies in humans demonstrated that olfactory function diminishes with increasing age (Ship et al. 1996), suggesting a possible decrease in the number of olfactory sensory neurons. Although the structure of both developing and mature olfactory epithelium (Farbman, 1994) have been well characterised, less information exists on changes relating specifically to ageing. A reduction in thickness of the olfactory epithelium was evident in ageing humans, with a concomitant loss of the normal zonal distribution of supporting and sensory cell nuclei, a less well defined boundary between respiratory and sensory epithelia, and an increase in pigment granules within the supporting cells (Naessen, 1971). Similar lysosome-like inclusion bodies were also noted in olfactory epithelium of adult rabbits (Mulvaney, 1971) and dogs over the age of 17 y (Hirai et al. 1996). Decreases both in the total area of olfactory epithelium and in dendritic knob density have been described in rats aged 29 mo and above (Hinds & McNelly, 1981). This is unlikely to be due to a loss of regenerative capacity since, in hamsters, regeneration of olfactory receptor neurons is observed in aged animals (Morrison & Costanzo, 1995). A scanning electron microscopic comparison of young and old rat olfactory epithelium revealed changes in membrane-limited dense bodies in olfactory receptor neuronal cell bodies (Naguro & Iwashita, 1992). In old rats (21 and 36 mo), large irregular bodies were found in the supranuclear area of olfactory receptor neurons and were also abundant throughout the sustentacular cells, resulting in cell enlargement and the loss of about 2 layers of olfactory receptor neuron perikarya. They contained lipid droplets and numerous irregular osmiophilic lamellae resembling lipofuscin granules (Naguro & Iwashita, 1992). No attempt was made to quantify these age related changes. The present study aimed to detail fully the morphological changes in the aged mouse olfactory epithelium and is a continuation of a previous pilot study (Appleton et al. 1996).

Type
Research Article
Copyright
© Anatomical Society of Great Britain and Ireland 1997

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