Abstract
Experimental evidence gathered over the last 6 years identifies two-pore K channel (K2P) family members as possible mediators of volatile anesthetic action. Earlier studies had identified a specific action of volatile anesthetics to enhance background potassium flux in excitable cells. Isolation of specific clones coding for background potassium channels–the K2P channel family–provided the molecular basis for these currents. Potentiation of currents passed by K2P channels by volatile anesthetics have been demonstrated in heterologous expression systems and in many sites in native excitable tissues. Recently, genetically altered mice in which the expression of one K2P channel (TREK-1) has been eliminated showed strong resistance to the action of volatile anesthetics. This accumulating evidence supports the hypothesis that enhancement of background currents passed by K2P channels underlie the action of volatile anesthetics.
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