title: Is anesthesia caused by potentiation of synaptic or intrinsic inhibition? Recent insights into the mechanisms of volatile anesthetics.
abstract: Volatile anesthetics modulate synaptic (GABAA receptor-mediated) and intrinsic (K+ channel-controlled) neuronal inhibition. GABAA receptor activity is enhanced, leading to increased charge transfer and prolonged synaptic inhibition, and members of the two pore domain family of potassium channels are activated, leading to neuronal hyperpolarization and reduced excitability. These effects may underlie different components of the complex anesthetic state.
authors.affiliation: Department of Anesthesiology, University of Wisconsin, Madison 53706, USA. mperouansky@facstaff.wisc.edu
authors.forename: M
authors.initials: M
authors.lastname: Perouansky
authors.forename: R A
authors.initials: RA
authors.lastname: Pearce
mesh_terms: D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D006801:Humans; D009433:Neural Inhibition / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects; D015221:Potassium Channels / Q000187:drug effects; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D013237:Stereoisomerism; D013569:Synapses / Q000187:drug effects* / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
chemical_list: D018685:Anesthetics, Inhalation; D015221:Potassium Channels; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid