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D Samigullin

Publications and source records attributed to D Samigullin.

4 recordsLinked to original sources

Calcium dependence of uni-quantal release latencies and quantal content at mouse neuromuscular junction.

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 m(o), 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), m(o) 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 m(o) 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 m(o) 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.

Action Potentials↗

Temperature effect on proximal to distal gradient of quantal release of acetylcholine at frog endplate.

The conduction velocity of the nerve terminal, mean quantal content, and release latencies of uniquantal endplate currents (EPCs) were recorded in proximal, central, and distal parts of the terminal by extracellular pipettes located 5, 50, and 100 microm from the end of myelinated nerve trunk. The spike conduction velocity, minimal latency, modal value of the latency histograms, and time interval during which 90% of EPCs released (P90) at distal, central, and proximal part of the frog nerve terminal have different temperature dependency between 10 degrees and 28 degrees C. As shown by the size and time-course of reconstructed multiquantal EPCs, the secretion synchronization, which is greatest in distal parts, compensates at least partly for the progressive slowing of spike conduction velocity in the proximodistal direction, in particular at lower temperatures.

Acetylcholine↗

Long release latencies are increased by acetylcholine at frog endplate.

Uni-quantal endplate currents (EPCs) were recorded extracellularly at the frog neuromuscular synapse and their latency dispersions expressed as P(90) 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 per cent of all measured uni-quantal EPCs had occurred, was significantly and reversibly increased by 66 per cent 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 per cent) in the amplitude of reconstructed multi-quantal currents.

Acetylcholine↗

Cyclic AMP synchronizes evoked quantal release at frog neuromuscular junctions.

At frog neuromuscular junction, noradrenaline (NA) shortens the release period for evoked quantal release acting on a beta1 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 1 x 10(-6) mol/l db-cAMP and 1 x 10(-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.

Acetylcholine↗