Acrylamide neurotoxicity in the mouse: a behavioral, electrophysiological and morphological study.
The development of acrylamide induced neurotoxicity was followed for 3 weeks in the mouse by behavioral testing, determination of conduction velocities and electron microscopic examination of peripheral nerves. Neurotoxic signs began to appear during the second week of treatment. A condition of severe intoxication developed within 21 days. Behavioral assessment for neurological deficits proved to be more sensitive than sensory or motor conduction velocity determinations either in isolated preparations or in situ. In general, such electrophysiological determinations did not result in reproducible, statistically significant, differences from control animals until the third week of acrylamide administration. However, there was a suggestion that temperature reduction may provide a provocative change to increase the sensitivity of such electrophysiological measurements. Electron microscopic examination of the nerves of severely poisoned animals revealed myelin corrugation and delamination to be the most consistent damage. Acrylamide appeared to produce a nonselective attack since degenerating fibers were found intermingled with almost normal fibers of approximately the same diameter. In general, the production of neurotoxicity in the mouse closely resembled that seen in the rat but some differences were noted.
D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D004594:Electrophysiology; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D009046:Motor Neurons / Q000187:drug effects; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects; D004856:Postural Balance / Q000187:drug effects; D011434:Proprioception / Q000187:drug effects; D012018:Reflex / Q000187:drug effects
D000178:Acrylamides