Non-quantal release of transmitter at mouse neuromuscular junction and its dependence on the activity of Na+-K+ ATP-ase.
The postjunctional membrane of mouse diaphragm fibres was hyperpolarized by 1-2 mV during local curarization of the end-plate zone in the presence of anticholinesterase. In a solution containing 5 mM K+, the mean hyperpolarization was 1.0+/-0.35 mV. Hyperpolarization was 1.46+/-0.30 mV when the activity of the Na-K pump was blocked by 2 x 10(-5) M ouabain and 1.82+/-0.43 mV when it was blocked by bathing the muscle in a K+-free medium. Reactivation of membrane ATP-ase by addition of potassium after a period in K+-free medium reduced the hyperpolarization to zero, when measurements were made 10-20 min after the readdition. It is concluded that spontaneous non-quantal leakage of acetylcholine occurs at the mouse neuromuscular junction, as it does in the frog (2). Conditions which block the Na+-k+-dependent ATPase increased the leakage whereas potentiation of the pump activity decreased it.
D000109:Acetylcholine / Q000378:metabolism*; D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D003964:Diaphragm; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009045:Motor Endplate / Q000502:physiology; D009469:Neuromuscular Junction / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014403:Tubocurarine / Q000494:pharmacology
D010042:Ouabain; D012964:Sodium; D000251:Adenosine Triphosphatases; D000109:Acetylcholine; D011188:Potassium; D014403:Tubocurarine