Maitotoxin activates quantal transmitter release at the neuromuscular junction: evidence for elevated intraterminal Ca2+ in the motor nerve terminal.
Maitotoxin (MTX), applied in vitro to the mouse neuromuscular junction, briskly activates the spontaneous release of acetylcholine quanta, manifest as miniature end-plate potentials (MEPPs). This effect requires external Ca2+ and is accompanied by a steady post-junctional depolarization. After the peak activation of the spontaneous release process, the quantal discharge gradually declines with eventual abolishment of MEPPs. In contrast to the striking increase in MEPP frequency, the quantum content of the nerve-evoked end-plate potentials (EPPs) is increased only moderately by MTX. These effects are attributable to the ability of the toxin to elevate the level of free intracellular Ca2+ in the motor nerve terminal. With further characterization of its presynaptic site of action, maitotoxin may become a useful tool in studying synaptic physiology.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D008387:Marine Toxins / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism; D035964:Oxocins; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects*; D000095702:Polyether Toxins
D000109:Acetylcholine; D002118:Calcium; D008387:Marine Toxins; D035964:Oxocins; C020394:maitotoxin; D000095702:Polyether Toxins