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[Ca.sub.2+]-induced [Ca.sub.2+] release (CICR) enhances a variety of cellular [Ca.sub.2+] signaling and functions. How CICR affects impulse-evoked transmitter release is unknown. At frog motor nerve terminals, repetitive [Ca.sub.2+] entries slowly prime and subsequently activate the mechanism of CICR via ryanodine receptors and asynchronous exocytosis of transmitters. Further [Ca.sub.2+] entry inactivates the CICR mechanism and the absence of [Ca.sub.2+] entry for [is greater than] 1 min results in its slow depriming. We now report here that the activation of this unique CICR markedly enhances impulse-evoked exocytosis of transmitter. The conditioning nerve stimulation (10-20 Hz, 2-10 min) that primes the CICR mechanism produced the marked enhancement of the amplitude and quantal content of end-plate potentials (EPPs) that decayed double exponentially with time constants of 1.85 and 10 min. The enhancement was blocked by inhibitors of ryanodine receptors and was accompanied by a slight prolongation of the peak times of EPP and the end-plate currents estimated from deconvolution of EPP. The conditioning nerve stimulation also enhanced single impulse- and tetanus-induced rises in intracellular [Ca.sub.2+] in the terminals with little change in time course. There was no change in the rate of growth of the amplitudes of EPPs in a short train after the conditioning stimulation. On the other hand, the augmentation and potentiation of EPP were enhanced, and then decreased in parallel with changes in intraterminal [Ca.sub.2+] during repetition of tetani. The results suggest that ryanodine receptors exist close to voltage-gated [Ca.sub.2+] channels in the presynaptic terminals and amplify the impulse-evoked exocytosis and its plasticity via CICR after [Ca.sub.2+]-dependent priming. KEY WORDS: [Ca.sub.2+]-induced [Ca.sub.2+] release * [Ca.sub.2+]-dependent priming * transmitter release * end-plate potential * frog motor nerve terminals