Effects of persistent sodium current blockade in respiratory circuits depend on the pharmacological mechanism of action and network dynamics
Fig 4
Phase plane representation of simulated TTX and RZ block of INaP in an isolated pre-BötC neuron.
(A) Vm- and hNaP-nullclines (black and gray, respectively) projected to the (Vm, hNaP)-plane under control conditions (gNaP = 5.0 nS) in a bursting regime, along with a projection of the bursting trajectory (blue). Note that this view does not represent the INaP activation variable mNaP. (B) Increasing TTX blockade of INaP moves the left knee of the Vm-nullcline to larger values of hNaP, which also abolishes bursting by creating a stable fixed point on the left branch of the Vm-nullcline via a SNIC (saddle-node on an invariant circle) bifurcation. (C) Increasing RZ blockade of INaP shifts the h-nullcline to the left, abolishing intrinsic bursting by creating a stable fixed point left branch of the Vm-nullcline, also via a SNIC bifurcation. gTonicE = 0.35 nS in all panels.