Propofol mechanism of action exerts its sedative hypnotic effects through a GABA receptor interaction. GABA is the principal inhibitory neurotransmitter in the CNS.
When GABAA receptors are activated, transmembrane chloride conductance increases, resulting in hyperpolarization of the postsynaptic cell membrane and functional inhibition of the postsynaptic neuron.
The interaction of propofol mechanism of action also etomidate and barbiturates with specific components of GABAA receptors appears to decrease the rate of dissociation of the inhibitory neurotransmitter GABA from the receptor, thereby increasing the duration of the GABA-activated opening of the chloride channel with resulting hyperpolarization of cell membranes.
Both immobilization and respiratory depression in propofol mechanism of action are mediated by beta3-containing GABAA receptors, hypnosis by both beta3- and beta2-containing GABAA receptors.
While the hypothermic, cardiac depressant and sedative actions are largely independent of beta3-containg GABAA receptors.
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