Axonal transport in neuropathy.
Recent studies on the distribution of labeled endogenous proteins in the experimental neuropathies induced by streoptozotocin diabetes, galactose feeding, zinc pyridinethione, 2,5-hexanedione, acrylamide, and p-bromophenylacetylurea (BPAU) have demonstrated an impaired build up of retrogradely transported material derived from the more distal parts of peripheral nerve. In BPAU neuropathy the transport abnormality is strongly related to the degree of muscle weakness; following treatment with acrylamide the extent of the impairment is dose related. In both toxic conditions the transport abnormality is present well in advance of the first clinical signs of neuropathy. We therefore suggest that changes in retrograde axonal transport play an initial and important role in the development of many axonopathies.
D020106:Acrylamide; D000178:Acrylamides / Q000494:pharmacology; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced / Q000378:metabolism*; D051381:Rats; D014508:Urea / Q000031:analogs & derivatives / Q000494:pharmacology
D000178:Acrylamides; D020106:Acrylamide; C004506:4-bromophenylacetylurea; D014508:Urea