Membrane Potential-Dependent Modulation of Recurrent Inhibition in Rat Neocortex
Figure 1
Modulation of slow (late-onset) disynaptic IPSP by presynaptic somatic Vm.
(A) Left, schematic diagram of the PC-PC paired recording (IN indicates those unidentified inhibitory interneurons that mediate the disynaptic IPSPs). Right, an AP burst (15 APs at 100 Hz) evoked by a train of current injection in PC1 induced a disynaptic response in PC2 with a long latency from the onset of the AP burst. * indicates individual IPSPs. (B) Example recording showing that presynaptic depolarization increased the amplitude of AP burst-induced disynaptic IPSPs. (C) Overlay of the IPSPs evoked at resting (blue) and depolarized (red) Vm in the presynaptic PC. Arrows indicate the onset of the AP train. Notice that presynaptic depolarization caused a reduction in failure, increased the amplitude, and shortened the latency of the disynaptic IPSPs. (D) Left, cumulative frequency distribution of the tested connections (n = 38 PC-PC pairs) by the average amplitude of disynaptic IPSP at resting (blue) and depolarized Vm (red); right, pooled results showing changes of the average amplitude at the two Vm levels in individual PC-PC pairs. (E) Pooled results (n = 38 pairs) showing that the onset latency of IPSPs was shortened by presynaptic depolarization. (F) The percentage increase was dependent on the average amplitude of disynaptic IPSPs (n = 38 pairs). Red line, hyperbolic fit. (G) Average time course of the facilitation in PC-PC pairs that showed significant increase in IPSP amplitude (n = 12 pairs tested). Error bars represent s.e.m. ** p<0.01.