Figure 6.

The “vulnerable brain” under anesthesia: a hypothesis linking metabolism, brain oscillations, burst suppression, and cognitive decline. Decreased astrocytic AG in prefrontal cortex fails to provide adequate metabolic support for neuronal oxidative phosphorylation (1) and sustained synaptic neurotransmission (2). Burst suppression is thought to occur when the brain has an inadequate supply of ATP. If metabolism is compromised as in (1) and (2), further depression of brain metabolism by anesthetic drugs via impaired mitochondrial function (3) results in a higher propensity for burst suppression. Astrocytes support brain metabolism, but are also thought to support brain oscillations through their highly connected syncytial networks. In the aging brain with preexisting neuromodulatory deficits, general anesthesia further inhibits subcortical neuromodulatory inputs on astrocyte syncytial networks (4) and suppresses astrocyte–neuron metabolic interactions, leading to less robust brain oscillations. Ach indicates acetylcholine; AG, aerobic glycolysis; ATP, adenosine triphosphate; NE, norepinephrine.