THE AGING OLFACTORY EPITHELIUM - NEUROGENESIS, RESPONSE TO DAMAGE, AND ODORANT-INDUCED ACTIVITY

Olfactory epithelium retains the capacity to recover anatomically afte r damage well into adult life and perhaps throughout its duration. Non e the less, olfactory dysfunctions have been reported widely for elder ly humans. The present study investigates the effects of aging on the neurophysiological and anatomical status of the olfactory epithelium i n barrier-raised Fischer 344X Brown Norway F1 hybrid rats at 7, 10, 25 and 32/35 months old. The posterior part of the olfactory epithelium in 32/35-month-old rats is well preserved. Globose basal cells are div iding, and new neurons are being born even at this advanced age. None the less, the numbers of proliferating basal cells and immature, GAP-4 3 (+) neurons are significantly decreased. Neurophysiological status w as evaluated using voltage-sensitive dye techniques to assess inherent patterns of odorant-induced activity in the epithelium lining the sep tum and the medial surface of the turbinates. In middle and posterior zones of the epithelium, there were neither age-related changes in ove rall responsivity of this part of the olfactory epithelium to any of f ive odorants, nor shifts in the location of the odorant-induced hotspo ts. The inherent activity patterns elicited by the different odorants do become more distinct as a function of age, which probably reflects the decline in immature neurons and a slight, but not statistically si gnificant, increase in mature neurons as a function of age. In contras t with the excellent preservation of posterior epithelium, the epithel ium lining the anterodorsal septum and the corresponding face of the t urbinates is damaged in the 32/35-month-old animals: in this part, hor izontal basal cells are reactive, more basal cells and sustentacular c ells are proliferating than in younger animals or in posterior epithel ium of the same animals, and the neuronal population is less mature on average. Our findings indicate that degeneration of the olfactory epi thelium is not an inevitable or preprogrammed consequence of the aging process, since the posterior zone of the epithelium is very well pres erved in these barrier-protected animals. However, the deterioration i n the anterior epithelium suggests that environmental insults can accu mulate or become more severe with age and overwhelm the regenerative c apacity of the epithelium. Alternatively, the regenerative capacity of the epithelium may wane somewhat with age. Either of these mechanisms or some combination of them can account for the functional and anatom ical deterioration of the sense of smell associated with senescence in humans. Copyright (C) 1996 ISDN.