Fig. 2: Synaptic targets of general anesthesia and its effect at the cellular scale, in experiments and modeling.
From: A computational approach to evaluate how molecular mechanisms impact large-scale brain activity
a, General anesthesia that targets GABAA receptors (for instance, propofol) prolongs IPSPs by increasing the opening duration of the chloride channels. We model this effect as an increase in the inhibitory synaptic decay time constant (τi). We illustrate the comparison of the model with whole-cell patch clamp recordings demonstrating the prolongation of IPSP caused by halothane. b, NMDA blockers (for instance, ketamine and xenon) decrease the duration of excitatory postsynaptic potentials (EPSPs), as shown by patch-clamp recordings of AMPA and NMDA currents under the effect of ketamine. This effect can be modeled as a decrease of the excitatory synaptic decay time constant (τe). Panels adapted with permission from: a(II) (top), ref. 61, Wiley; b(II) (top), ref. 62, MIT Press.
