title: Abnormalities of axonal transport: are they a cause of peripheral nerve disease?
abstract: Applications of pulse-labeling techniques to the study of axonal transport have provided new insights into certain types of peripheral nerve disease. In normal neurons, many of the newly synthesized proteins that are rapidly transported to distal parts of the cell eventually undergo a process of "turnaround," after which they are carried back to the cell bodies for degradation. This turnaround is selectively impaired in rat nerves early in the course of streptozotocin-induced diabetes and of experimental neuropathies induced by exposure to acrylamide, zinc pyridinethione, or p-bromophenylacetylurea. In the neuropathy of p-bromo-phenylacetylurea, depression of turnaround precedes the clinical signs of neurologic dysfunction, is later proportional to the severity of the disability, and may account for the characteristic accumulation of debris in preterminal axons.
mesh_terms: D000178:Acrylamides; D000818:Animals; D001370:Axonal Transport; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D006801:Humans; D009119:Muscle Contraction; D009121:Muscle Denervation; D009410:Nerve Degeneration; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D009942:Organometallic Compounds; D010523:Peripheral Nervous System Diseases / Q000209:etiology*; D011725:Pyridines; D051381:Rats; D013311:Streptozocin; D014508:Urea / Q000031:analogs & derivatives
chemical_list: D000178:Acrylamides; D009419:Nerve Tissue Proteins; D009942:Organometallic Compounds; D011725:Pyridines; C004506:4-bromophenylacetylurea; D013311:Streptozocin; D014508:Urea; C010423:pyrithione zinc