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. 2020 Mar 12;9:e53281. doi: 10.7554/eLife.53281

Figure 3. Feedback inhibition from GGN extends the dynamic range of KCs.

(a) Model schematic: A single KC sends 50,000 excitatory synapses with random delays of 0–60 ms into GGN’s α lobe branch. The KC receives feedback inhibition via a graded synapse from GGN’s calyceal branch. A step current is injected into the KC from 0.5 to 3 s (up to 2 s is shown). (b) The model KC was tested with current pulses of increasing amplitude in three configurations: Isolated KC (left); KC receiving only spontaneous inhibition from GGN (middle), and KC receiving spontaneous and odor-elicited feedback inhibition (right). As the amplitude of the current pulse increases, the KC’s spiking first increases, and then, as the membrane potential nears saturation, decreases. (c) Comparison of the number of spikes evoked by current steps in KC in the three configurations shown in b). (d) Slopes of the rising parts of the KC-only (left, cyan) and KC with GGN feedback (right, orange) curves in c), normalized by the KC-only slope.

Figure 3.

Figure 3—figure supplement 1. Model KC responses to current step injections while inhibited by pseudo-dynamic clamp of GGN voltage from a network model show inhibition expands dynamic range of KCs.

Figure 3—figure supplement 1.

The test KC received no inhibition (left column), inhibition driven by weak GGN depolarization (middle column), or strong GGN depolarization (right column). The strong GGN voltage was obtained from the simulation of a full PN-KC-GGN network model. The weak GGN depolarization was derived by halving the deflections of the former from resting potential.