Fig. 10.

Synaptic inhibition in normal saline. The HN(L,4) cell was voltage-clamped while the contralateral HN(R,4) cell was driven by the HN(3) cells via the HN(1,2) cells. A, Normal activity in the HN(4) cells. The action potentials of the HN(R,4) cell were monitored with a loose patch electrode on the cell soma, and each spike in the HN(R,4) cell is marked above the intracellular record of the HN(L,4) membrane potential. B, The inhibitory synaptic current from the HN(R,4) cell to the HN(L,4) cell shown while voltage-clamping the HN(L,4) cell at −55 mV. The spike-mediated IPSCs occurred on top of graded inhibitory synaptic current. Below the recorded current trace, two traces show the slow oscillation in the current. The trace with the largest amplitude is a low-pass-filtered version of the HN(L,4) current (moving average over 50 msec), and the trace with the smallest amplitude is the current immediately before spike-mediated inhibitory currents (baseline current, seeC). A few spikes escaped voltage control during the noninhibited phase simultaneously with electrical EPSPs from the HN(X) cell (Calabrese, 1977). C, Expanding the first cycle inB. Each spike in the HN(R,4) cell gives rise to a spike-mediated IPSC in the HN(L,4) cell. The difference between the recorded current and the baseline of the spike-mediated IPSCs (thick trace) shows the contribution of the fast spike-mediated IPSCs to the total synaptic inhibition (also inB). A few extra IPSCs from the HN(L,1) and HN(L,2) cells can be seen between the IPSCs from the HN(R,4) cell. The insetshows three IPSCs on a 5× expanded time scale as well as the low-pass-filtered current (upper thick line) and the baseline current (lower thick line). D, The amplitude of the spike-mediated IPSCs in the postsynaptic HN(L,4) cell was modulated. The time indicated was from the first spike in the bursts. The histogram comprises IPSCs from nine successive bursts, has a binwidth of 300 msec, and each bin up to 3.5 sec contained >20 spikes.