[Effects of chronic paralysis of chick embryo by flaxedil on the development of the neuromuscular junction].
Chronic paralysis of Chick embryos by the cholinergic antagonist flaxedil blocks the subsynaptic accumulation of acetylcholinesterase but not the formation of acetylcholine receptor cluster. Flaxedil paralysis also causes an increase of the total muscle content of acetylcholine receptor without altering the half-life of the receptor protein. The spontaneous activity of the embryon therefore "shuts off" the synthesis of extrasynpatic acetylcholine receptor.
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D002642:Chick Embryo; D002908:Chronic Disease; D005703:Gallamine Triethiodide / Q000494:pharmacology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D010243:Paralysis / Q000139:chemically induced / Q000503:physiopathology*; D011950:Receptors, Cholinergic / Q000378:metabolism
D011950:Receptors, Cholinergic; D000110:Acetylcholinesterase; D005703:Gallamine Triethiodide
Effets de la paralysie chronique de l'embryon de poulet par le flaxédil sur le développement de la jonction neuro-musculaire.