Recent research has revealed new electrophysiological oscillations that are associated with unconsciousness under general anesthesia. We are using biophysical modeling to elucidate how the molecular actions of anesthetic drugs manifest in larger neuronal networks to create such brain dynamics. As an example, I will first present recent modeling of an 'alpha' (9-12Hz) EEG oscillation that appears during surgical levels of propofol-induced general anesthesia. Such oscillations differ from classical 'alpha' oscillations in their frequency and spatial location. Using conductance-based neuronal models, we have shown how propofol - an agonist of GABAergic neurotransmission - can promote highly synchronous alpha oscillations in thalamocortical networks, leading to the observed phenomenology. These oscillations may impede normal thalamocortical dynamics and thus, correlate with reductions in arousal.

I will then discuss recent models for the state of burst suppression, which consists of high voltage EEG activity (bursts) that alternates with isoelectric quiescence (suppression). Burst suppression occurs at deep levels of general anesthesia and also in pathological conditions such as coma. Our modeling suggests that the dynamics of burst suppression arise not simply from neuromodulatory effects, but also from changes in brain metabolism. Specifically, I will discuss how a lowered cerebral metabolic rate can lead to epochs of burst and suppression by inducing transient reductions in cerebral ATP and subsequent gating of neuronal potassium channels. This model provides a unified mechanism of burst suppression that is consistent with each of its etiologies and provides a platform to study the brain network dynamics associated with other anesthetic drugs and related pathological states.