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 frog neuromuscular junction, noradrenaline (NA) shortens the release period for evoked quantal release acting on a b 1 receptor. To test the hypothesis that this action of NA is mediated by cAMP, we measured the latencies of focally recorded uni-quantal endplate currents (EPCs) after application of dibutyryl-cAMP (db-cAMP) and adenylyl cyclase activator, forskolin. The interval between the time when responses with minimal delay appeared and the point at which 90 % of all latencies had occurred (P90 parameter) was shortened in the presence of both 1x10-6 mol/l db-cAMP and 1x10-6 mol/l forskolin by about 30 %. The cAMP-induced shortening is equal to that found after application of NA and effects of both drugs are not additive., E. Bukcharaeva, D. Samigullin, E. E. Nikolsky, F. Vyskočil., and Obsahuje bibliografii
Uni-quantal endplate currents (EPCs) were recorded extracellularly at the frog neuromuscular synapse and their latency dispersions expressed as P90 were estimated in the presence of acetylcholine. Stimulation-evoked EPCs with long release latencies increased in number when acetylcholine was applied. P90, which is designated as the interval between the minimal synaptic delay and the time at which 90 % of all measured uni-quantal EPCs had occurred, was significantly and reversibly increased by 66% from 0.51 ms to 0.85 ms in the presence of 5x10-4 M acetylcholine. This indicates that the evoked release pattern is less synchronous and the increased asynchrony leads to a substantial drop (by 28%) in the amplitude of reconstructed multi-quantal currents., D. Samigullin, E. A. Bukharaeva, E. Nikolsky, S. Adámek, F. Vyskočil., and Obsahuje bibliografii