Journa Lof Neurophysiology

I. We examined high-threshold synaptic transmission between oscillatory pairs of leech heart interneurons. Inhibitory postsynaptic currents ( IPSCs) could be reliably evoked by depolarizing the presynaptic neuron in voltage clamp from a holding potential of -35 mV. At this presynaptic potential, the Ca2+ currents underlying graded transmission are completely inactivated, and we conclude that a high-threshold Ca2+ current is extant in heart interneurons. Further evidence for this was that inhibitory postsynaptic currents were blocked when Co2+ replaced Ca2’ in the saline and thus high-threshold transmission was dependent on the presence of external Ca2+. 2. When IPSCs were evoked by a 200-ms duration voltage step from a holding potential of -35 mV in the presynaptic neuron, the time course of turn-on of the IPSC consisted of a fast (time-topeak = 17.5 t 1.93 (SE) ms [n = 71) and a slow (time-to-peak = 250 t 28.5 ms [n = 81) component. FMRF-NH, reduced the amplitude of the fast component but did not affect the slow component. When the presynaptic voltage step was ended the IPSC turned off with a single exponential time course. FMRF-NH, slowed the time course of turn-off of the IPSC. 3. When IPSCs were evoked by a 1500-ms duration voltage step from a holding potential of -35 mV in the presynaptic neuron, these IPSCs peaked around 300 ms. Following the peak, the IPSC decayed with a single exponential time course. FMRF-NH, accelerated the time course of this decay. At potentials of 0 mV and +5 mV, FMRF-NH, produced a significant decrease in the peak current and at potentials of -5 mV and 0 mV, produced a significant decrease in the current integral. 4. High-threshold IPSCs could also be evoked by a spike in the presynaptic neuron. Bath application of 1 PM FMRF-NH, decreased the amplitude of the spike-evoked IPSC and slowed the time course of its falling phase. 5. We examined the effect of FMRF-NH, on the quanta1 synaptic transmission. Bath-application of FMRF-NH, increased binomial p, the probability of release, and decreased binomial n, the number of units available for release. FMRF-NH, had no effect on 4, the unit size, when calculated from the distributions of PSPs, and increased the coefficient of variation (CV). 6. The lack of a change in 4 and the increase in CV suggested that FMRF-NH, acted at a presynaptic location. We applied acetylcholine, the transmitter between heart interneurons, focally to the somata of these neurons and found that FMRF-NH, produced no change in the response of these cells to applied transmitter. 7. We produced a computer model of a heart interneuron having only a leak conductance, Ih, the hyperpolarization-activated inward current, and the high-threshold synaptic conductance. Results of the modeling suggest that FMRF-NH, may produce its effects on the heart rhythm by interactions of its effects on highthreshold transmission with both Ih and low-threshold Ca2+ currents.