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1. FDNB increased by 60-90% the depolarization of the end-plate produced by applied carbachol in frog sciatic nerve-sartorius muscle preparations.
2. In partially curarized preparations, FDNB (0·4 mM) increased the amplitude of the end-plate potential by a factor of 1·8.
3. The quantal content of end-plate potentials was increased by FDNB (2 mM) as determined by the method of failures.
4. After approximately 25-35 min, neuromuscular transmission was blocked by 0·4 mM-FDNB, as evidenced by abolition of neurally elicited end-plate potentials. At this stage miniature end-plate potentials could still be recorded, which indicates that the neuromuscular block was presynaptic.
5. FDNB (0·4 mM) increased miniature end-plate potential frequency several hundred-fold when the Ringer solution contained normal calcium concentration (1·8 mM) or 0·45 mM calcium and 5·4 mM magnesium.
6. During the first 60 min of exposure to 0·4 mM-FDNB there was a slight drop (4-6 mV) in resting potentials of muscle fibres. During this period directly initiated action potentials showed a marked decrease in the rate of repolarization and a small decrease in the amplitude and rate of rise.
7. Using the technique of point voltage clamping in tetrodotoxin-treated muscles, it has been found that FDNB almost completely abolished the active increase in gK during stepwise depolarization of the nonjunctional muscle fibre membrane from -90 to 0 mV. The passive outward leakage current appeared unaffected by FDNB.
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