title: Facilitation and impulse propagation failure at the frog neuromuscular junction.
abstract: Exposure of frog neuromuscular junctions to solutions which contain a high concentration of calcium ions produces failure of neuromuscular transmission. This failure of transmission is abrupt and usually complete. However, some terminals produce small end-plate potentials even after the exposure to a high concentration of calcium ions. A second stimulus to the nerve can overcome the block of neuromuscular transmission if the interval between the stimuli is less than a critical value. The size of the end-plate potential is almost independent of the interstimulus interval if the latter is less than the critical value but more than the refractory period. The depth of this neuromuscular block is affected by temperature, potassium ions, osmotic pressure, cobalt ions, and prior high frequency stimulation of the nerve. Neuromuscular transmission failure coincides with failure of the nerve action potential (NAP) to invade the terminal. Prior to propagation failure, the second extracellularly recorded NAP is smaller, but is conducted faster than the first NAP. The relevance of these findings to the facilitation of transmitter release seen in solutions of normal divalent ion content is discussed.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003035:Cobalt / Q000494:pharmacology; D005110:Extracellular Space; D009045:Motor Endplate / Q000187:drug effects; D009468:Neuromuscular Diseases / Q000139:chemically induced; D009469:Neuromuscular Junction / Q000502:physiology*; D009997:Osmotic Pressure; D011188:Potassium / Q000494:pharmacology; D011894:Rana pipiens; D013268:Stimulation, Chemical; D009435:Synaptic Transmission; D013696:Temperature; D013997:Time Factors
chemical_list: D003035:Cobalt; D011188:Potassium; D002118:Calcium