Pre‐ and post‐ junctional effects of 1‐fluoro‐2,4‐dinitrobenzene at the frog neuromuscular junction

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 g K during stepwise depolarization of the nonjunctional muscle fibre membrane from −90 to 0 mV. The passive outward leakage current appeared unaffected by FDNB.