General anesthetics work by altering the activity of specific neurons in the brain. One main class of these drugs, which includes propofol and the ether-derivative sevoflurane, work primarily by increasing the activity of inhibitory GABAA receptors, while a second class that includes ketamine primarily blocks excitatory NMDA receptors.
The GABAA receptor is a channel that allows chloride ions to flow into the neuron, decreasing the voltage within the cell relative to the extracellular space. Such hyperpolarization decreases the probability that the neuron will fire. Propofol and sevoflurane increase the chloride current going into the cell, making the inhibition more potent.
The NMDA receptor allows sodium and calcium ions to flow into the cell, while letting potassium ions out, increasing the voltage within the cell relative to the extracellular space and increasing the probability of neural firing. Ketamine blocks this receptor, decreasing its excitatory actions.
Anesthetics’ interactions with neural receptors alter ...
