We have studied the effect of the
biogenic amines,
serotonin and
dopamine, on post-tetanic potentiation (PTP) at an identified synapse in the abdominal
ganglion of Aplysia californica. We found that: (1) 10(-7) M perfused
serotonin doubles the rate constant of decay of PTP. The effect is specific in that neither the size of the non-potentiated (isolated) EPSP nor the amplitude of PTP is affected. As reported previously, higher doses of
serotonin will also increase the amplitude of PTP and decrease the size of the isolated EPSP; (2) 5 X 10(-7) M
dopamine in the perfusate increases the rate constant of decay of PTP by about 50%. The effect is also specific in that neither PTP amplitude nor the size of the isolated EPSP is affected; (3) SQ10,631, a
serotonin antagonist, blocks the effect of perfused
serotonin on PTP decay rate. It does not antagonize the
dopamine effect. SQ10,631 also slows the endogenous decay of PTP in some preparations which exhibit an unusually fast PTP decay rate, suggesting a naturally occurring source of
serotonin within the
ganglion capable of affecting the rate constant of PTP decay; (4) (+)-
butaclamol, a
dopamine antagonist, blocks the effect of
dopamine on the rate constant of PTP decay, whereas (-)-
butaclamol has little effect.
Butaclamol does not block the effect of
serotonin on the rate constant of PTP decay; (5)
phosphodiesterase inhibitors potentiate the effect of
serotonin on the rate constant of PTP decay, and
cyclic AMP analogues mimic the effect of the
biogenic amines, suggesting that the aminergic modulation of the rate of decay of PTP is coupled with activation of
adenylate cyclase and accumulation of
cyclic AMP; and (6) the evidence presented is consistent with the hypothesis that
serotonin and
dopamine are capable of specifically modifying the rate of change in the efficacy of transmitter release which underlies PTP. It also suggests that the two
biogenic amines operate separately and in parallel via
presynaptic receptor mechanisms.