The following is one of the many elegant statements in General Anesthetic Actions on GABAA Receptors:
It is the fervent view of the authors that general anesthesia is no different from any other pharmacological process: exogenously administered drugs interact with key sites on cellular proteins in the body which results directly in the alteration in the function of these proteins, in the present case, neuronal proteins that control how information is conveyed through the nervous system.
Isoflurane, Sevoflurane, and Desflurane, the current inhalation general anesthetics, along with Halothane and the intravenous anesthetics Propofol, Etomidate, Methohexital and Thiopental, enhance the function of GABAA receptors (GABAARs), the most abundant fast inhibitory neurotransmitter receptor in the CNS (ligand-gated chloride ion channels) by increasing the affinity of the receptor for GABA. Since these receptors are abundant in parts of the CNS that process higher-order brain functions, it stands to reason that GABAAR function is central to memory, awareness and consciousness. GABAARs are involved in mediating hypnosis, depression of spinal reflexes, and amnesia, three of the classical components of general anesthesia. Isoflurane, Sevoflurane, and Desflurane enhance the amplitude of responses to low concentrations of GABA and prolong the duration of GABA mediated synaptic inhibition.
A very good starting point for your investigations can be found by clicking on the linked article above.
Agent-selective effects of volatile anesthetics on GABAA receptor-mediated synaptic inhibition in hippocampal interneurons
The sedative component of anesthesia is mediated by GABA(A) receptors in an endogenous sleep pathway