Abstract
Olfactory receptor cells are continuously replaced throughout the lifetime of vertebrates, including mammals. Basal cells divide and give rise to new receptor cells which project their axons to the olfactory bulb, where they make contact with mitral/tufted cells and periglomerular cells. After bulbectomy the rate of cell division is increased in the olfactory epithelium for at least 50 days after surgery. The increased rate of proliferation is related to premature
death of receptor ceHs, presumably because they lack a trophic substance provided by the bulb. We asked whether the mitral cells this putative trophic substance. In 18 day old rats (PI 8), mitral cells were selectively damaged unilaterally by cutting their axons in the lateral olfactory tract. Before killing at P40, P66 and P105, rats were injected with [3H]thymidine or bromodeoxyuridine to label dividing cells. We determined the proliferative rate of neurons in olfactory epithelium by counting a cumulative 80 mm linear span of olfactory epithelium on the ipsiand
contralateral sides of operated animals, and control
unoperated animals of the same age. Tractotomy resulted in a 26\% reduction in the number of mitral cells on the operated side. Electron microscopic examination of surviving mitral/tufted cells indicated a reduction in size and reduction in amount of rough endoplasmic reticulum. The olfactory epithelium on the operated side in all three experimental groups showed a 21\% increase in the number of cells incorporating the DNA label, compared with that on the unoperated side. Values from the unoperated side did not
differ from those in unoperated controls. The results indicate that the loss or damage of mitral cells influences the proliferative rate of olfactory receptor cells, possibly by reducing their average life span.
