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Factors influencing an increase in spontaneous transmitter release by hypoxia at the mouse neuromuscular junction.

To test a possibility that the functional buffering of intracellular Ca2+ plays a primary role in the enhancement of spontaneous transmitter release during hypoxia, the frequency of miniature end‐plate potentials (m.e.p.p.s) was examined under several conditions. At 36 degrees C, hypoxia (bubbling with 95% N2 and 5% CO2) increased the average frequency of m.e.p.p.s from about 3 s‐1 to 100 s‐1 or more, in a standard Krebs‐Ringer solution. This effect declined with a decrease in the temperature and was much reduced at 24 degrees C. Removal of external Ca2+ (addition of 2 mM‐EGTA), increase of Mg2+ levels to 5 mM, and treatment with 20 microM‐ouabain, which gave a slight increase, did not reduce the rise in m.e.p.p. frequency during hypoxia. Pre‐incubation of the tissue in a solution containing 10 mM‐KCl at 24‐32 degrees C and its subsequent exposure to hypoxia caused a very marked increase in m.e.p.p. frequency, while incubation in 10 mM‐KCl alone caused a small rise in the frequency. These data indicate that this combination potentiates the individual effects of each treatment. These experiments suggest that the hypoxia‐induced increase in spontaneous transmitter release is primarily due to an increase in intracellular Ca2+ levels, probably because of inhibition of mechanisms which control buffering and extrusion of intracellular Ca2+. The release and influx mechanisms which elevate intraterminal Ca2+ may also be involved passively in the effect of hypoxia.