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• W78998972 abstract "Volatile anesthetics induce neuron hyperpolarization and consequent depression of the central nervous system (Nicoll and Madison, 1982; Berg- Johnsen and Langmoen, 1987; Franks and Lieb, 1988; el-Beheiry and Puil, 1989; Southan and Wann, 1989; Maclver and Kendig, 1991; Franks and Lieb, 1994; Harris et al, 1995; Belelli et al, 1999; Sirois et al, 2000). Besides the well known potentiation of GABAA and glycine chloride channels (Harris et al, 1995; Belelli et al, 1999), evidence demonstrates that in both vertebrates and invertebrates, volatile anesthetics open background K channels and thus increase the resting membrane potential (Franks and Lieb, 1988; Winegar et al, 1996; Lopes et al, 1998; Sirois et al, 2000). For instance, in the mollusc Lymnea, halothane opens a class of baseline K+ channels (IKAn) which hyperpolarize and silence pacemaker neurons (Franks and Lieb, 1988; Franks and Lieb, 1991; Lopes et al, 1998). In Aplysia californica, halothane-mediated neuronal hyperpolarization is due to the opening of the background S type (serotonin-sensitive) K+ channel (Winegar et al, 1996). Similarly, opening of baseline acid-sensitive K+channels by volatile anesthetics produces rat hypoglossal and locus coeruleus neuron hyperpolarization (Sirois et al, 1998; Sirois et al, 2000)." @default.
• W78998972 created "2016-06-24" @default.
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• W78998972 date "2003-01-01" @default.
• W78998972 modified "2023-10-01" @default.
• W78998972 title "2P Domain K+ Channels: Novel Pharmacological Targets for Volatile General Anesthetics" @default.
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• W78998972 doi "https://doi.org/10.1007/978-1-4419-9280-2_2" @default.
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