FIG. 4.

Effect of GABA_A receptor agonists on the response of regular spiking (RS) neuron model in pathological brain states, in the presence and absence of Na⁺-K⁺-2Cl^- (NKCC1) co-transporter blockers. (A) Response of the RS neuron model to GABA_A receptor agonists in an epileptic brain state. The values of extracellular potassium and intrcellular chloride are shown in the upper panel. Under these epileptic conditions, GABA_A receptor agonists can still help hyperpolarize the neuron, as would be expected from their common use as anti-epileptic drugs. (B) Same as in A, but for a post-traumatic brain injury (TBI) brain state. The GABA_A agonist is unable to rescue the neuron from depolarizaiton block. (C) Response of the RS neuron model to a combination of GABA_A receptor agonist and NKCC1 co-transporter blocker in a post-TBI brain state. Dotted line signifies the change in intracellular chloride caused by the effect of the NKCC1 co-transporter blocker. The combination of the two drugs is able to rescue the model neuron from depolariziation block.