Figure 7.

The pre-POC stimulation amplitude of AB inhibition is not sufficient to elicit pyloric-timed activity in MCN1 after POC stimulation. A, After POC stimulation, natural AB inhibition suppresses MCN1 activity, resulting in a pyloric-timed MCN1 firing pattern. Replacing the natural AB inhibition of MCN1 with dynamic-clamp AB (dAB) inhibition injected at the pre-POC amplitude is not sufficient to reliably suppress MCN1 firing, although it does modulate the MCN1 firing frequency. Using the post-POC amplitude, dAB inhibition injected into MCN1 does successfully suppress MCN1 firing, causing pyloric-timed MCN1 activity similar to that occurring in response to natural AB inhibition. B, The percentage of MCN1 action potentials per bin and the phase of AB/PD activity (box) are plotted against the normalized pyloric cycle for three conditions: natural AB inhibition of MCN1, plus pre- and post-POC amplitude dAB inhibition of MCN1. In response to natural AB inhibition and post-POC amplitude dAB inhibition, there is a decrease in the percentage of MCN1 spikes occurring during the initial 35% of the normalized pyloric cycle relative to pre-POC dAB inhibition. The effect of dAB inhibition begins earlier in the normalized pyloric cycle than the natural AB inhibition because there is only a brief delay (∼5 ms) from the onset of the dAB burst in the dynamic-clamp software to the injection of dAB inhibition into MCN1. In contrast, there is a conduction delay of ∼25 ms for the natural AB spikes to travel from the STG to each CoG (Blitz and Nusbaum, 2008). The horizontal bars indicate the region of statistical analysis. Schematics to the right of each panel indicate whether natural AB inhibition was present or dAB inhibition was injected into MCN1. The arrows indicate that MCN1 voltage is read into, and dAB current is sent out from the dynamic-clamp software. Error bars indicate SEM. *p < 0.05 compared with natural AB; ^#p < 0.05 compared with pre-POC dAB.