Sodium channel localization in rat sciatic nerve following lead-induced demyelination.
Daily intraperitoneal injections of lead acetate for several weeks were followed by a peripheral neuropathy. The conduction of impulses in the sciatic nerve became slower, but their amplitude, duration and threshold remained normal. Sodium channel labeling with specific monoclonal antibodies revealed staining at demyelinated regions, while normal axons were stained exclusively at nodes of Ranvier. These results support the view that remodelling of sodium channel distribution may contribute to impulse conduction in demyelinated fibers.
H
H
Meiri
S
S
Pri-Chen
A D
AD
Korczyn
D000818:Animals; D000911:Antibodies, Monoclonal; D003711:Demyelinating Diseases / Q000139:chemically induced* / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D007473:Ion Channels / Q000378:metabolism*; D007854:Lead / Q000633:toxicity*; D009431:Neural Conduction; D009942:Organometallic Compounds; D010525:Peripheral Nerves / Q000378:metabolism*; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced* / Q000378:metabolism; D051381:Rats
D000911:Antibodies, Monoclonal; D007473:Ion Channels; D009942:Organometallic Compounds; D007854:Lead; C008261:lead acetate