Action mechanisms of intravenous anesthetics
Berg-Johnsen, J.
Tidsskrift for den Norske Laegeforening Tidsskrift for Praktisk Medicin Ny Raekke 113(5): 565-568
1993
ISSN/ISBN: 0029-2001 PMID: 8096655 Document Number: 417530
Intravenous anaesthetic agents depress the activity of the brain by acting on receptor-operated ion channels. Barbiturates enhance gamma-aminobutyric acid (GABA)-mediated inhibition, depress glutamate-mediated excitation, and hyperpolarize the membrane by increased potassium conductance. Benzodiazepines facilitate GABA-mediated inhibition by binding to a benzodiazepine recognition site on the GABA receptor complex, and affect potassium channels. Opioids bind to opioid receptors and hyperpolarize the membrane by enhanced potassium and calcium conductances. Ketamine depresses excitatory synaptic transmission by acting on glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype. Propofol acts at a recognition site on the GABA receptor, which differs from the binding sites of both barbiturates and benzodiazepines.