Olfactory disturbance induced by deafferentation of serotonergic fibers in the olfactory bulb.

The serotonergic neurons of the brain stem project widely throughout the central nervous system, and the olfactory bulb is one of the major forebrain targets of the ascending serotonin pathway. According to physiological studies, neurons of the olfactory bulb were found to reduce their spontaneous discharge rates by electrophoretically applied serotonin. However, roles of the bulbar serotonin in the sense of smell remain unanswered. In the present study, using 5,7-dihydroxytryptamine, a specific neurotoxin for serotonin, we found that the conditioned rats who learned to avoid a repellent by olfaction lost ability of discrimination by deafferentation of the bulbar serotonergic fibers. Such olfactory dysfunction did not occur in the early stage (three days after injection of the toxin) when the serotonergic fibers disappeared in the bulb, but developed a few weeks later. Interestingly, histological examination revealed marked shrinkage of the bulbar glomerulus which is a major termination site of the bulbopetal serotonergic fibers, and also a synaptic site of olfactory receptor cells and bulbar output neurons. The results indicate that depletion of the serotonergic fibers in the olfactory bulb causes glomerular atrophy and olfactory disturbance in the rat.