Amplitude and rate of decay of post-tetanic potentiation are controlled by different mechanisms.
Evidence is presented that post-tetanic potentiation (PTP) of the cholinergic, fast, Cl- dependent IPSP seen in cell L5 of the abdominal ganglion of Aplysia californica upon eliciting a spoke in cell L10 is due to an increase in spike-evoked transmitter release. The magnitude of the post-tetanic change in spike-evoked release is inversely correlated with the amount of transmitter released by an isolated presynaptic spike. This was found whether the latter was increased by injection of tetraethyl ammonium (TEA) into the soma of L10 or decreased by hyperpolarization of the soma of L10. Neither of these manipulations affected the rate of decay of PTP. The magnitude of PTP was increased and the rate of decay reduced by increasing either the number or frequency of stimuli in the tetanus. Under all conditions PTP decayed with a single exponential time course, asymptotically approaching the unpotentiated magnitude. It is concluded that while both the amplitude and rate of decay of PTP are affected by the frequency and number of stimuli in the tetanus, the underlying mechanism controlling the amplitude of PTP is different from the mechanism controlling the rate of decay of PTP.
Amplitude and rate of decay of post-tetanic potentiation are controlled by different mechanisms. Evidence is presented that post-tetanic potentiation (PTP) of the cholinergic, fast, Cl- dependent IPSP seen in cell L5 of the abdominal ganglion of Aplysia californica upon eliciting a spoke in cell L10 is due to an increase in spike-evoked transmitter release. The magnitude of the post-tetanic change in spike-evoked release is inversely correlated with the amount of transmitter released by an isolated presynaptic spike. This was found whether the latter was increased by injection of tetraethyl ammonium (TEA) into the soma of L10 or decreased by hyperpolarization of the soma of L10. Neither of these manipulations affected the rate of decay of PTP. The magnitude of PTP was increased and the rate of decay reduced by increasing either the number or frequency of stimuli in the tetanus. Under all conditions PTP decayed with a single exponential time course, asymptotically approaching the unpotentiated magnitude. It is concluded that while both the amplitude and rate of decay of PTP are affected by the frequency and number of stimuli in the tetanus, the underlying mechanism controlling the amplitude of PTP is different from the mechanism controlling the rate of decay of PTP.