Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory Effects
Fig 4
PAD-mediated inhibition in a neuron model.
(A) 2-D bifurcation diagram showing the combinations of EGABA and p associated with PAD-induced spiking (grey region) and PAD-mediated inhibition of other spiking (green region), where p represents the proportion of sodium channels susceptible to inactivation. Simulations here are based on a neuron model with sodium channel inactivation (Eq 7) with βw = 0 mV and ḡGABA = 2 nS/pF. Note that the green and grey regions overlap, indicating that PAD can initiate its own spikes yet still inhibit spikes initiated by other means (e.g. by stimulating current Istim). Labels a-e indicate parameter combinations for which sample responses are shown in B. (B) Responses to gGABA steps occurring alone or during Istim steps are shown down the left and right columns, respectively. (C) Boundary between inhibitory and non-inhibitory region (as in A) re-plotted for different ḡGABA. Higher ḡGABA enables GABA to be inhibitory despite less inactivating sodium current (i.e. smaller p) and more depolarized EGABA.