Uni-quantal endplate currents (EPC) were recorded at mouse diaphragm neuromuscular synapse by extracellular microelectrode during motor nerve stimulation. The probability of release expressed as quantal content mo, and variability of synaptic latencies expressed as P90
were estimated in the presence of extracellular calcium ([Ca2+]o)
varying between 0.2 and 0.6 mM in the bathing solution. At 0.2 mM [Ca2+]o, mo was low (0.10) and many of long-latency EPCs were present during the late phase of the release (P90 = 2.44 ms). No change in mo was found when [Ca2+]o was 0.3 mM, but P90
decreased by 39 %. For latency shortening, saturating concentration of [Ca2+]o was 0.4 mM, when P90 was 1.49 ms and latencies did not further change at 0.5 and 0.6 mM [Ca2+]o. In the latter concentrations, however, an increase of mo was still observed. It can be concluded that the early phase of the secretion did not significantly change when [Ca2+]o was raised and that only the late phase of the release depends on extracellular
calcium up to 0.4 mM.
At 20oC, both quantal and non-quantal spontaneous acetylcholine release (expressed as miniature endplate potential frequency [f-MEPPs] and the H-effect, respectively) increased during the first 30 min of hypoxia in solution with normal extracellular calcium ([Ca2+]o = 2.0 mM). The hypoxia-induced tenfold increase of the f-MEPPs was virtually
absent in low calcium solution ([Ca2+]o = 0.4 mM) whereas there was still a significant increment of non-quantal release. This indicates that each of these two processes of acetylcholine release is influenced by mechanisms with different oxygen sensitivity. The rise of f-MEPPs during the onset of hypoxia apparently requires Ca2+ entry into the nerve terminal, whereas the non-quantal release can be increased by another factors such as a lower level of ATP.