Decrease of the spontaneous non-quantal release of acetylcholine from the phrenic nerve in botulinum-poisoned rat diaphragm.
Botulinum type A toxin (BoTx) has been found to diminish by 40% the spontaneous release of acetylcholine (ACh) from normal (acutely denervated) rat diaphragms incubated in the presence of 5 mM K+, while the release of ACh from chronically (4 days) denervated diaphragms was not affected during 2 h incubations. The toxin has been found to rapidly remove (within 10 min) the local depolarization of about 8 mV which developed in the end-plate zones of the diaphragms after the inhibition of cholinesterases; after the administration of BoTx, tubocurarine lost its ability to increase the resting membrane potential (H-response, Katz and Miledi 1977) in the end-plate area of anticholinesterase-treated muscles. It is concluded that BoTx inhibits the non-quantal release of ACh from the motor nerve fibres and that it probably acts directly on the nerve terminal surface membrane (without internalization). The H-response in the rat diaphragm reflects the non-quantal release of ACh from the nerve terminals and not from the muscle fibres.
D000109:Acetylcholine / Q000032:analysis / Q000378:metabolism*; D000818:Animals; D001905:Botulinum Toxins / Q000506:poisoning*; D003964:Diaphragm / Q000032:analysis / Q000378:metabolism*; D004594:Electrophysiology; D005260:Female; D006181:H-Reflex; D066298:In Vitro Techniques; D010791:Phrenic Nerve / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D001905:Botulinum Toxins; D000109:Acetylcholine