Disruption of axonal transport from olfactory epithelium by 3-methylindole.

The effects of 150, 350, and 400 mg/kg intraperitoneal 3-methylindole (3-MI) on anterograde transport of horseradish peroxidase from the olfactory epithelium to the olfactory bulb were investigated. In 400 mg/kg 3-MI-treated rats sacrificed after 7 days only about 2% of all glomeruli had normal levels of the reaction product, and most glomeruli had no detectable reaction product. Lower doses of 3-MI produced correspondingly less disruption of axonal transport, with savings located primarily in the ventral to midlateral and the ventromedial region of the bulb. There was a gradual recovery of bulbar connections in 12-, 22-, and 92-day survival rats. In all cases, the increase in axonal transport was greatest in glomeruli on the lateral, ventral, and ventromedial areas of the bulb, and least evident or absent on the dorsal and dorsomedial areas.

Odor detection in rats with 3-methylindole-induced reduction of sensory input.

Rats were tested on odor-detection tasks after treatment with 400 mg/kg of 3-methyl-indole. As revealed by anterograde transport of horseradish peroxidase from the olfactory epithelium to the olfactory bulb glomeruli, treatment produced a severe (>97%) loss in sensory input relative to untreated controls. In almost all cases, only glomeruli in a restricted ventromedial segment of the bulb contained control levels of reaction product. In Experiment 1, five of nine experimental rats were anosmic or severely hyposmic, but the remaining four rats were able to detect amyl acetate vapor. In Experiment 2, four of seven experimental rats were anosmic, but the remaining three were able to detect each of four different odors. Among all experimental rats, those that were anosmic had significantly fewer glomeruli with dense anterograde transport than did those that could smell. Among rats that could smell, performance accuracy was related to the number of glomeruli with reaction product.