Chronic impairment of axonal transport eliminates taste responses and taste buds.

A Silastic nerve cuff containing colchicine (1% w/v) was placed around the combined lingualchorda tympani nerve of the Mongolian gerbil (Meriones unguiculatus) to evaluate the role of axonal transport in the maintenance of taste buds. After 3 days the summated gustatory impulse discharges recorded from the chorda tympani nerve were reduced by 60%, while compound action potentials had not changed appreciably. The lingual-chorda tympani nerve underwent ultrastructural changes including a loss of microtubules, an increased prominence and disorientation of neurofilaments, and a significant shrinkage in the cross-sectional area of axoplasm. The shrinkage of axoplasm and the accumulation of mitochondria and cholinesterase at the nerve cuff provided evidence that the colchicine treatment acted to impair axonal transport. More substantial pathological changes were evident in nerve ultrastructure by 15 days when both the ipsilateral chorda tympani taste responses and fungiform taste buds were nearly absent. Control cuffs lacking colchicine had little effect on chorda tympani taste responses, taste buds, or nerve ultrastructure. Eight or 15 days of nerve exposure to lumicolchicine, an isomer of colchicine with low affinity for tubulin, had no significant effect on taste responses. [3H]Colchicine was used in the nerve cuff to demonstrate that colchicine must have acted directly upon the nerve trunk, rather than the taste buds, to cause the loss of taste responses and taste buds. [3H]Colchicine levels were equal in the two sides of the tongue, whereas both the functional and structural deterioration of the taste buds were restricted to the ipsilateral side. We conclude that the loss of taste responses and taste buds was caused by chronically impaired axonal transport in gustatory axons.