Effects of acrylamide and other sulfhydryl compounds in vivo and in vitro on staining of motor nerve terminals by the zinc iodide-osmium technique.
The zinc iodide-osmium technique blackens motor nerve terminals by selectively staining synaptic vesicles. Intraperitoneal injections of acrylamide (30 mg/kg/day, 5 times each week) cause inhibition of staining by this technique so that approximately one third of the end-plates in rat sternocostalis muscle are unstained after 24 hours, and by 17 days more than 70% are unstained. This is not associated with nerve fiber degeneration. A similar inhibition of staining can also be shown after prior incubation of the sternocostalis muscle in 4 mM acrylamide in oxygenated Ringer's solution. Intraperitoneal injection of the thiol group blocker N-ethylmaleimide also causes marked inhibition of staining of motor end-plates by this method. Dithiothreitol, which prevents the oxidation of thiol groups, will partly prevent the inhibition of staining by both acrylamide and N-ethylmaleimide, when given in vivo.
D020106:Acrylamide; D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D002415:Cats; D004229:Dithiothreitol / Q000633:toxicity*; D005033:Ethylmaleimide / Q000633:toxicity*; D005260:Female; D009045:Motor Endplate / Q000187:drug effects* / Q000378:metabolism; D009132:Muscles / Q000294:innervation / Q000378:metabolism; D009469:Neuromuscular Junction / Q000187:drug effects*; D009992:Osmium / Q000378:metabolism*; D009993:Osmium Tetroxide; D051381:Rats; D011919:Rats, Inbred Strains; D013194:Staining and Labeling; D015032:Zinc / Q000378:metabolism*; D017967:Zinc Compounds
D000178:Acrylamides; D017967:Zinc Compounds; D020106:Acrylamide; D009992:Osmium; C035252:osmium zinc iodide; D015032:Zinc; D005033:Ethylmaleimide; D009993:Osmium Tetroxide; D004229:Dithiothreitol