Fig. 3: Spike frequency adaptation and post-inhibitory rebound.
a Schematic of the modified circuit to demonstrate spike frequency adaptation by mimicking calcium-activated potassium channel (KCa). A diode D0 in series with a capacitor CCaK (marked in red) lead to a non-linear, delayed rise in hyperpolarizing current with help of the transistor TL. b Raster plot showing spike frequency adaptation by simulating the circuit in (a) for a range of amplitudes (200–600 pA) of the Isyn pulses. ISI increases with time, or in other words, spike frequency reduces. c Instantaneous ISI and current through TL (ITL) as a function of time for 500 pA Isyn pulse. ITL emulates both leakage current (IL) and KCa current (ICaK). ISI−1 decreases and saturates to a lower value in response to an increase in ITL. d Instantaneous ISI−1 as a function of time similar to (c) for the data in (b). The data is fitted with an exponential decay function to extract initial spike frequency (f0), steady-state spike frequency (fss) and the decay time constant (tSFA). Adaptation factor (fadap) is calculated as \((f_0-f_{{{ss}}})/f_0\). e Plots showing parameters extracted from (d) with Isyn. As expected, f0 increases with Isyn with lower fss values. tSFA does not vary with Isyn as expected, and fadap increases with Isyn suggesting a limit on the spike rate because of ICaK. f Functionally, the same components (D0-CCaK) also help elicit a rebound signal after an inhibitory (negative) current input. VM plot after the end of a −100 pA Isyn pulse shows spike generation. Inset shows increasing post-inhibitory rebound in VM for lower Isyn magnitudes (10–30 pA) which fail to generate spikes. g Raster plot showing spike timing for inhibitory Isyn magnitudes. The number of spikes and ISI−1 increase with increasing negative Isyn. The time of the last spike occurrence with respect to end of inhibitory input is recorded as tend. h Peak ISI−1 and tend increase reaching saturation with more negative Isyn. Saturation in tend and its similarity to tSFA reaffirms the role of D0-CCaK in evoking post-inhibitory rebound.
