Long‐term potentiation of transmitter release induced by repetitive presynaptic activities in bull‐frog sympathetic ganglia.

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Abstract
Long-lasting potentiation of transmitter release induced by repetitive presynaptic activities in bullfrog sympathetic ganglia was studied by recording intracellularly fast excitatory postsynaptic potentials (fast EPSP). Following a brief period of post-tetanic potentiation or depression (less than 10 min), the amplitude of the fast EPSP was potentiated for a period between several tens of minutes and more than 2 h in response to tetanic stimulation of the preganglionic nerve in 21 out of 28 cells. Quantal analysis revealed that this long-term potentiation (LTP) of the fast EPSP was accompanied by an increase in quantal content m (in 9 out of 21 cells), quantal size (4 cells) or both (8 cells). The increased quantal content (presynaptic LTP) declined exponentially (10 cells) or decayed gradually to a certain enhanced level which lasted several hours. The increased quantal size grew with a relatively long latency (10-25 min) and remained relatively constant for at least 2 h. The magnitude of presynaptic LTP increased with increased duration of the presynaptic tetanus (33 Hz) from 2-5 s. No LTP was elicited by a 1-s tetanus, whereas the time course appears to be independent of the tetanus duration and the magnitude of LTP. There was a positive correlation between the magnitude of presynaptic LTP and the pre-tetanic quantal content up to m = 3, but the former deviated from linear regression when the value of the latter exceeded 3. No LTP occurred when quantal content was less than 0.5. A tetanus (33 Hz, 10 s) applied in Ca2+-free solution elicited no presynaptic LTP, while the same tetanus in normal Ringer solution produced a large presynaptic LTP. Presynaptic LTP was enhanced in magnitude at low temperature (8-10.degree. C). A use-dependent, long-term potentiation of transmitter release occurs in bull-frog sympathetic ganglia. Several possible mechanisms are discussed in terms of Ca2+-buffering mechanisms of the presynaptic nerve terminals.