Short-term modulation of endogenous bursting rhythms by monosynaptic inhibition in Aplysia neurons: effects of contingent stimulation.

A presynaptic neuron fires a high-frequency train of spikes that produces long-lasting synaptic inhibition that modulates the bursting rhythm in a small population of endogenous bursting neurons in the left upper quadrant of the isolated abdominal ganglion of Aplysia. Single inputs decrease or increase the duration of the burst cycle as a function of the precise phase of the input (the phase response curve). Two phases of the burst cycle were used to analyze the effects of repeated contingent (phase-locked) stimulation. One contingency involved synaptic input early in the burst cycle that inhibited spikes and decreased the duration, whereas the other contingency involved input late in the cycle that increased the duration. Under both contingencies of stimulation, buildup and short-term persistence were found, however these cumulative effects were not dependent upon the phase of the burst cycle. The locus of the short-term plasticity that underlies the buildup and persistence is in the pacemaker properties of the postsynaptic cell rather than in the synapse. The plastic change appears to involve a nonspecific postinhibitory rebound that follows a single input and builds up with repetition. These results support the suggestion that endogenous rhythms of pacemaker cells can undergo plastic changes and can therefore serve as a means of short-term information storage in the nervous system. However, this neuronal circuit does not have the specificity required to mediate operant conditioning.