Journal of Neuroscience, Vol 3, 117-123, Copyright © 1983 by Society for Neuroscience
Chronic impairment of axonal transport eliminates taste responses and taste buds
HE Sloan, SE Hughes and B Oakley
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.