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- C S Yost, A T Gray, B D Winegar, and D Leonoudakis.
- Department of Anesthesia, University of California, San Francisco 94143, USA.
- Toxicol. Lett. 1998 Nov 23;100-101:293-300.
AbstractA large body of evidence has accumulated in recent years pointing towards the GABA(A) receptor as a primary determinant of volatile anesthetic action (Franks and Lieb, 1994). Nevertheless, our understanding of the function of the central nervous system (CNS) remains sufficiently incomplete that other mechanisms of CNS depression remain to be examined. We have studied a new family of potassium (K+) channels which function as regulators of the baseline excitability of neuronal tissue. As such they must be considered potential targets for volatile anesthetic action and as a possible mechanism by which volatile anesthetics act to allow patients to undergo noxious surgical stimulation.
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