MECHANISM OF ACTION OF GENERAL-ANESTHETICS - EFFECT ON IONIC CHANNEL PROTEINS OR ON MEMBRANE PHOSPHOLIPIDS

General anesthesia is defined by reversible unconsciousness, lack of r esponse to noxious stimuli, and amnesia, induced by chemical agents. M echanisms underlying the anesthetic effect are not known. The most pre valent belief was that anesthetic drugs acted on the lipid cell membra nes, based on the correlation between oil solubility and anesthetic po tency. Later, it has been proposed that anesthetic agents act on speci fic proteins of eht cellular membrane of neurons. Voltage-gated ionic channels are inhibited by anesthetic agents, being some subtypes more sensitive. Clinical concentration of anesthetic agents inhibit or stim ulate excitatory or inhibitory neurotransmitter receptors, respectivel y. Specific receptor agonists and antagonists modify this effect. Inte rcellular channels (gap junctions) are also affected by anesthetic age nts through direct interaction with some of their protein subunits. Th us, anesthesia would result from combined effects on specific proteins acting on neural cell excitability as well as transmission and propag ation of nerve impulses.