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Following unilateral olfactory bulbectomy in rats the ipsilateral olfactory neuroepithelium undergoes degeneration. Subsequently, the receptor neuron complement of the tissue is restored by the proliferation and differentiation of immature neuroblasts. However, as noted by other workers, in the absence of a target organ the dynamics of neuron regeneration is altered such that there is an overall reduction in the number of cells positive for the olfactory marker protein when cellular equilibrium is re-established. Immunocytochemical staining of the olfactory epithelium of unilaterally bulbectomized rats with a series of anti-neuronal monoclonal antibodies reveals an attenuation of binding of some antibodies to the neurons of the ipsilateral epithelium. In contrast, other anti-neuronal monoclonal antibodies show no difference in staining intensity when ipsilateral and control contralateral epithelia are compared. These data suggest that the expression of some neuronal antigens is subject to control by the target olfactory bulb, whereas others are independent of such putative regulation. Besides altering the expression of some antigenic determinants, olfactory bulbectomy also results in certain organizational changes in epithelium. First, bulbectomy produces an increase in the incidence of a cell type that appears to span the neuroepithelium. Although the morphology of these cells is more akin to a sustentacular cell than to a receptor neuron, they are not immunoreactive with antibodies to sustentacular cells. The cells are stained, however, by an anti-neuronal antibody, NEU-9. The second aspect of altered organization is the appearance of novel olfactory marker protein-positive structures in the olfactory mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Monoclonal antibodies reveal novel aspects of the biochemistry and organization of olfactory neurons following unilateral olfactory bulbectomy