Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory Effects
Fig 1
PAD-induced spiking in a neuron model.
(A) 2-D bifurcation diagram showing the combinations of EGABA and βw that allow a GABA conductance step (ḡGABA = 2 nS/pF) to elicit repetitive or transient spiking (dark and light grey regions, respectively). Labels a-f indicate parameter combinations for which sample responses are shown in B. Normal conditions correspond to EGABA = -35 mV and βw = -20 mV (point b). (B) Sample responses to a fast synaptic waveform (τrise = 2 ms, τdecay = 20 ms), a slow synaptic waveform (τrise = 20 ms, τdecay = 200 ms) and a conductance step for parameter combinations labeled in A. Slow-onset conductance requires stronger ḡGABA (3.5 nS/pF, grey trace in c) to elicit transient spiking than a fast-onset conductance; all black traces are for ḡGABA = 2 nS/pF. (C) 2-D bifurcation analysis described in A was repeated for different ḡGABA values. Dashed and solid lines show borders for the transient and repetitive spiking regions, respectively. Increasing ḡGABA from 1 to 2 nS/pF (cyan → black) caused a downward shift in both borders but further increases (black → green) caused little change in the former and a rightward shift in the latter, indicating that increased ḡGABA confers increased spiking only to a certain point, beyond which further increase actually reduces spiking.