Long‐term potentiation induced by a sustained rise in the intraterminal Ca2+ in bull‐frog sympathetic ganglia.

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Abstract
1. The mechanism of a long‐term potentiation of transmitter release (pre‐LTP) induced by a tetanic stimulation (33 Hz for 1‐30 s) applied to the preganglionic nerve was examined by intracellularly recording the fast excitatory postsynaptic potentials (fast EPSPs) in bull‐frog sympathetic ganglia. 2. Short‐term facilitation induced by paired pulses was decreased during the course of pre‐LTP; the extent of reduction paralleled with the magnitude of pre‐LTP. 3. The frequency of miniature EPSPs increased after tetanic stimulation that produced the pre‐LTP. 4. The Ca2+ ionophore, A23187, increased both the amplitude and quantal content of fast EPSPs and frequency of miniature EPSPs while it decreased short‐term facilitation. 5. A Ca2+ chelating agent, Quin‐2, loaded as acetoxymethyl ester, reduced the amplitude and quantal content of fast EPSPs and short‐term facilitation, and blocked the generation of pre‐LTP. 6. Activators of protein kinase C, phorbol 12,13‐dibutyrate and 1‐oleoyl‐2‐acetyl‐rac‐glycerol, and its inhibitors, H‐7 and staurosporine, did not block the generation of pre‐LTP, while the activators enhanced transmitter release. 7. Inhibitors of calmodulin, trifluoperazine and W‐7, blocked the generation of pre‐LTP, whereas the amplitude and quantal content of fast EPSPs were not influenced. 8. These results suggest that the pre‐LTP results from a sustained rise in the basal level of intraterminal Ca2+ and an activation of the Ca(2+)‐calmodulin‐dependent process in the preganglionic nerve terminals.