In botulinum type A-poisoned frog motor endings ouabain induces phasic transmitter release through Na+-Ca2+ exchange.
Ouabain (100 microM) applied for 60 min to botulinum A (BoTx) poisoned motor junctions increases, in a time-dependent manner, the mean number of acetylcholine quanta released by nerve stimulation and enhances the delayed transmitter release. The drug does not affect spontaneous quantal release. The observed effects on evoked transmitter release cannot be explained by changes in the configuration of presynaptic currents recorded from motor terminals. They suggest that in BoTx-poisoned motor endings the level of intraterminal Ca2+, lower than that required for the activation of quantal transmitter release, can be effectively increased through the reversed operation of an Na+-Ca2+ exchange system that normally uses the Na+ gradient to extrude Ca2+.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001905:Botulinum Toxins / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D010042:Ouabain / Q000494:pharmacology*; D011896:Rana temporaria; D012964:Sodium / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger; D009435:Synaptic Transmission / Q000187:drug effects*
D002352:Carrier Proteins; D019831:Sodium-Calcium Exchanger; D010042:Ouabain; D012964:Sodium; D001905:Botulinum Toxins; D000109:Acetylcholine; D002118:Calcium