Datensatz

Zusammenfassung

Background: In cultured slice preparations of rat neocortical tissue, clinically relevant concentrations of volatile anesthetics mainly decreased action
potential firing of neurons by enhancing gamma-aminobutyric acid (GABA(A)) receptor- mediated synaptic inhibition. The author's aim was to determine if
other anesthetic agents are similarly effective in this model system and act via the same molecular mechanism. Methods: The actions of various general
anesthetics on the firing patterns of neocortical neurons were investigated by extracellular single-unit recordings. Results: Pentobarbital, propofol ketamine, and
ethanol inhibited spontaneous action potential firing in a concentration-dependent manner. The estimated median effective concentration (EC50) values were
close to or below the EC50 values for general anesthesia, Bath application of the GABA(A) antagonist bicuculline (100 mu M) decreased the effectiveness of
propofol, ethanol halothane, isoflurane, enflurane, and diazepam by more than 90, indicating that these agents acted predominantly via the GABA(A)
receptor. The depressant effects of pentobarbital and ketamine mere not significantly reduced by bicuculline treatment, Drugs acting mainly via the GABA,
receptor altered the firing patterns of neocortical cells in different manners. Diazepam reduced the discharge rates by decreasing the number of action potentials
per burst, leaving the burst rate unaffected Ln contrast, muscimol, GABA, propofol, and volatile anesthetics decreased the burst rate. Conclusions: Although
several anesthetic agents acted nearly exclusively via the GABA(A) receptor, they changed the discharge patterns of cortical neurons in different ways. This
finding is explained by GABA-mimetic or benzodiazepine-like molecular interactions.