CHANGES IN EXPRESSION OF THE LOW-AFFINITY RECEPTOR FOR NEUROTROPHINS,P75(NGFR), IN THE REGENERATING OLFACTORY SYSTEM

We have disrupted the integrity of the rat olfactory neuroepithelium u sing intranasally applied TX-100, a procedure known to reversibly elim inate the sensory neuron input from the neuroepithelium to the olfacto ry bulb [Margolis et al. (1974) Denervation in the primary olfactory p athway of mice: biochemical and morphological effects. Brain Res. 81, 469-483]. One week after TX-100 exposure, we observed a disruption of the pseudo-stratified organization of the neuroepithelium which was ac companied by a 60% reduction in neuroepithelial width, compared to sal ine-treated controls. Full recovery of the neuroepithelium was not obs erved until 16 weeks post-lesion. During this post-lesion period, we m onitored the expression of the low affinity receptor for neurotrophins , p75(NGFR), in the olfactory bulb of saline- and TX-100-treated anima ls, using the monoclonal antibody, MAb192. In saline-treated animals, p75(NGFR)-immunoreactivity (p75(NGFR)-ir) was localized to individual glomeruli in the olfactory bulb, with little or undetectable p75(NGFR) -ir in the olfactory nerve layer. We have previously reported that pre -lesioned levels of p75(NGFR)-ir in the glomerular layer were dramatic ally reduced while an induction of p75(NGFR)-ir was observed in the ol factory nerve layer, one and two weeks after intranasal exposure to TX -100 [Turner and Perez-Polo (1992) Regulation of the low affinity rece ptor for nerve growth factor, p75(NGFR), in the olfactory system of ne onatal and adult rat. Int. J. Devl Neurosci. 10, 343-359]. In this pap er, we demonstrate that this previously reported reduction in glomerul ar p75(NGFR)-ir took 16 weeks to fully recover and was, thus, coincide nt with the post-lesion recovery of the neuroepithelium. In the olfact ory nerve layer, the return of p75(NGFR)-ir to pre-lesioned levels too k only four weeks. No changes in neuroepithelial width and integrity o r alterations in p75(NGFR)-ir in the olfactory bulb were observed in s aline-treated animals. Thus, the TX-100-induced removal of the periphe ral input to the olfactory bulb resulted in a reversible change in exp ression of p75(NGFR)-ir in the bulb. We believe that these changes are a reflection of the regenerative capacity of the olfactory system.