Temperature‐sensitive aspects of evoked and spontaneous transmitter release at the frog neuromuscular junction.

Abstract

The temperature dependence of presynaptic processes involved in neuromuscular transmission was studied by rapidly increasing the temperature of cooled frog neuromuscular junctions by 4.degree.-10.degree. C using pulses from a neodymium laser. The temperature elevation was complete within 0.5 ms, and decayed back to control levels with a time constant of about 7-8 s. Temperature jumps completed before nerve stimulation increased the quantal content and decreased the latency of the end-plate potential (EPP). The Q10 for EPP quantal content in low [Ca2+] Ringer averaged about 3.9 over the range 1-18.degree. C. Temperature jumps occurring during the synaptic delay (the interval between the presynaptic action potential and the onset of the EPP) also increased the quantal content and decreased the latency of the EPP. The magnitude and timing of evoked release are influenced by temperature-sensitive processes that operate both during and shortly after the presynaptic nerve action potential, but are largely complete before the onset of release. Temperature jumps were applied at various times during the interval between 2 nerve stimuli. The amplitude of the 2nd EPP decreased as the temperature jump was moved earlier in the interstimulus interval, suggesting that the rise in temperature following the 1st nerve stimulus accelerates the decay of facilitation. When the temperature jump was moved from 10 ms after to 10 ms before the onset of the 1st EPP, the amplitude of the 2nd EPP either decreased or showed no change. Temperature jumps immediately accelerated the time course of spontaneous miniature end-plate potentials (mepp) and increased their frequency. The marked difference in Q10 for spontaneous transmitter release under different experimental conditions suggests that not all transmitter release uses identical mechanisms. A possible explanation for these variations in temperature sensitivity is that the activation energy and temperature sensitivity of quantal transmitter release is high when intracellular [Ca2+] is low, and that an increase in intracellular [Ca2+] (caused, for example by nerve stimulation or high [K+] in the presence of Ca2+, low temperature or injury to the nerve terminal) catalytically reduces this activation energy, thus increasing the rate and reducing the temperature sensitivity of quantal transmitter release. Calculations show that such a Ca2+-induced reduction in the activation energy would be more than sufficient to account for the acceleration of transmitter release observed following nerve stimulation.