Veratridine-induced high-frequency asynchronous release of inhibitory transmitter quanta in crayfish nerve-muscle synapses superfused with normal and low-calcium saline.

Crayfish fibres of opener muscles were voltage clamped to E = -80 mV membrane potential (T = 19-22 degrees C), and veratridine (10-100 mumol/l) was added to the superfusate. Within 30-60 s this caused large fluctuations of the clamp current due to vigorous asynchronous quantal release from the inhibitory nerve terminals along the muscle fibre. Excitatory postsynaptic receptors were previously desensitized by application of 5 mmol/l glutamate. Current fluctuations were evaluated by means of the noise analysis technique. Typically, 100 mumol/l veratridine increased instantaneously the quantal release rate n from n less than 1 quantum/s to n congruent to 10,000 quanta/s. Thereafter, n declined exponentially with a time constant of congruent to 70 s. On average, about 500,000 inhibitory quanta could be liberated in this way from the terminals on a single muscle fibre of congruent to 1 mm length. Serotonin (1 mumol/l) facilitated the effect of lower veratridine concentrations (1-10 mumol/l). In opener muscles veratridine-induced asynchronous quantal release showed little dependence on the bath concentration of Ca2+. The opposite was found for fibres of the superficial abdominal extensor muscle. Beside postsynaptic current fluctuations, veratridine elicited slowly changing average postsynaptic DC-currents which could be explained partly by superposition of individual inhibitory quantal currents. These DC-currents suggest that beside inhibitory quantal release another factor activates inhibitory postsynaptic receptors after application of veratridine.