Juxtaglomerular (JG) neurons of rat olfactory bulb (OB) have been shown to express tyrosine hydroxylase (TH), the rate-limiting enzyme in the catecholamine synthesis pathway. These JG neurons act as inhibitory dopaminergic interneurons, modulating the incoming signal from the primary olfactory afferents. The JG neurons, comprised of periglomerular, external tufted, and short axon cells, stop expressing TH after lesions of the olfactory nerve or closure of the nares, both of which cause a loss of functional input. Upon reinnervation by a continuously regenerating olfactory nerve, these cells resume their expression of TH. In order to study deafferentation and subsequent reinnervation within this system, our laboratory utilizes a transplantation model. Sections from transplant (TX) OBs are reacted for TH using immunocytochemical localization protocols and studied by light- and especially electron microscopy (EM). Autoradiography of tritiated thymidine-labeled tissue was performed to confirm donor origin of the TX OBs. Although the architecture of the TX OB is somewhat disrupted and the TH-positive cells were not as uniform in their arrangement as they are in the normal OB, we found that the TH cells in the TH OB had a morphology similar to the JG cells observed in normal OB. These TH cells were also found to receive synaptic contacts with host olfactory nerve axons as well as make and receive contacts with the processes of donor neurons. These, synaptic contacts were formed within areas that resemble the glomeruli of normal olfactory bulb, suggesting that the inhibitory synaptic pathway is reestablished within the TX OB. These findings also suggested that host olfactory axons formed a functional contact with the TH cells, possibly inducing them to express this enzyme. This study implies that the TX OB retains a level of plasticity that enables it to recapitulate part of the interneuronal arrangement observed in the normal system.