Following chemically induced peripheral deafferentation of the main olfactory bulb, expression of the low affinity receptor for neurotrophins, p75NGFR, was monitored immunohistochemically using monoclonal antibody MAb192. In control animals, p75NGFR expression was localized to the glomerular layer of the main olfactory bulb and deepest one third of the olfactory neuroepithelium. Peripheral lesioning dramatically reduced expression of glomerular p75NGFR while inducing expression of p75NGFR in the olfactory nerve layer. Expression of p75NGFR in the lesioned neuroepithelium was disorganized compared with controls. These observations demonstrate that the maintenance of the peripheral input from the neuroepithelium is critical to expression of p75NGFR in the main olfactory bulb.