Development of olfactory marker protein and tyrosine hydroxylase immunoreactivity in the transplanted rat olfactory bulb.

Evidence suggests that tyrosine hydroxylase (TH) expression by juxtaglomerular (JG) neurons of the olfactory bulb (OB) is dependent upon input from primary olfactory neurons (ONs), which are identifiable using immunocytochemical localization (ICC-L) methods for olfactory marker protein (OMP). When the input from the continuously regenerating ONs is temporarily removed (either surgically or chemically), JG cells cease TH production until ON contact is reestablished. We are studying this transneuronal regulation using the rat OB in a transplantation (TX) model. Fetal OBs, labeled in utero with tritiated thymidine, were transplanted (TX) into a site vacated by removal of a neonatal host OB. Host animals were sacrificed at varying periods after TX. Alternate sets of frozen sections were then processed for autoradiography or using ICC-L for TH and OMP. As early as 1 week post-TX, OMP-positive fibers and glomerulus-like structures were seen throughout the TX OB. Despite this extensive and rapid OMP reinnervation, TH expression returned very slowly and the number of TH expressing cells never approached control levels. The reduced TH activity in TXs may be due to failure of JG cells to survive or to develop the correct phenotype under TX conditions. Alternatively, input from ON fibers may only be necessary, but not sufficient, for the expression of TH.