Fig 5. Propofol gGABAA potentiation enables sustained alpha by changing the balance of excitation and inhibition.
(A) Representative TC voltage traces for the same gH-background excitation state under either baseline spindling (green trace) or high-dose propofol sustained alpha (red trace). (B) Zoom of A around T-current de-inactivation window. Baseline spindles terminate from H-current up-regulation, which raises the minima of TC cell voltage outside the T-current de-inactivation window. Under high-dose propofol gGABAA potentiation, the TC cell voltage floor does not rise from the window. (C) Representative TC cell T-current de-inactivation state variables (hT) for baseline and high-dose. Note that baseline spindles stop spiking once the hT maxima are below a threshold. (D) Representative TC cell H-current magnitude of baseline and high-dose. Note that baseline spindles stop spiking once H-current magnitude is high enough, but high-dose sustained alpha continues to spike even with a stronger realized H-current. (E) gH-background excitation plane for baseline simulations. (F) gH-background excitation plane for high-dose propofol simulations. (G) Illustration of the intrinsic TC-RE oscillation cycle; propofol gGABAA potentiation and negative background excitation enhance the RE burst inhibition, while H-current and positive background excitation augment the time from TC voltage minimum to TC bursting. (H) Representative TC voltage traces for the same gH-background excitation state under either baseline silent depolarization (blue trace) or high-dose propofol sustained alpha (red trace). (I) Zoom of H around T-current de-inactivation window; baseline never enters the T-current window, and therefore does not oscillate. (J) Representative TC cell T-current de-inactivation state variables for baseline and high-dose. (K) Representative TC cell H-current magnitude of baseline and high-dose.