Effects of the facilitatory compounds catechol, guanidine, noradrenaline and phencyclidine on presynaptic currents of mouse motor nerve terminals

Catechol, guanidine, noradrenaline, and phencyclidine can increase acetylcholine release at neuromuscular junctions. To determine if they act by affecting nerve terminal action potentials, the electrical activity of the terminal regions of motor nerves was recorded with an extracellular electrode inserted in the perineural sheaths of nerves in the mouse triangularis sterni preparation. Catechol (from 10 microM) and guanidine (from 1 mM) produced a selective reduction in the component of the perineural waveform associated with voltage-dependent K+ currents, without significant effects on Na+, Ca2+, or Ca2+-activated K+ currents. A selective block of K+ channels in nerve terminals would cause a prolonged depolarization and hence a large influx of Ca2+ to trigger acetylcholine release; this could explain the facilitatory effects of guanidine and catechol. Noradrenaline produced a slight increase in the amplitude of the perineural waveform. This is consistent with hyperpolarization of the resting membrane potential of the nerve, which could lead to facilitation of acetylcholine release. Phencyclidine blocked Na+- and K+-related portions of the signal.