Previously, we have shown that erbB-3 expression is restricted to the enshe
athing cells of the olfactory nerve layer, while erbB-4 is found in the per
iglomerular and mitral/tufted cells of the olfactory bulb and in cells comi
ng out from the rostral migratory stream of the subependymal layer. In the
present work, we have treated adult mice with zinc sulfate intranasal irrig
ation and analyzed erbB-3 and erbB-4 expression in the deafferented olfacto
ry bulb. Following treatment, olfactory axons undergo degeneration, as indi
cated by the loss of OMP expression in the deafferented olfactory bulb. The
thickness of the olfactory nerve layer is reduced, but the specific intens
ity of erbB-3 labeling in the remaining olfactory nerve layer is increased
with respect to control. Interestingly, following deafferentation, erbB-4 i
mmunoreactivity decreases specifically in cell types that normally make syn
aptic contacts with primary olfactory neurons in the glomeruli, i.e. perigl
omerular and mitral/tufted cells. Partial lesion of the olfactory epitheliu
m allows regenerative axon growth of olfactory neurons to the olfactory bul
b. Following olfactory axon regeneration, erbB-3 and erbB-4 immunoreactivit
y in the olfactory bulb is similar to control. Thus, like tyrosine hydroxyl
ase, the down regulation of erbB-4 expression in the periglomerular cells i
s reversible.