The shaker potassium channel is no target for xenon anesthesia in short-sleeping Drosophila melanogaster mutants.

BACKGROUND:Xenon seems to be an ideal anesthetic drug. To explore if next to the antagonism at the NMDA-receptor other molecular targets are involved, we tested the xenon requirement in short sleeping Drosophila shaker mutants and in na[har(38)]. METHODS:The Drosophila melanogaster strains wildtype Canton-S, na[har(38)], sh(102) and sh(mns), were raised and sleep was measured. Based on the response of the flies at different xenon concentrations, logEC50 values were calculated. RESULTS:The logEC50-values for WT Canton-S were 1.671 (1.601-1.742 95%-confidence intervall; n = 238; P versus sh(102) > 0,05), for sh(mns) 1.711 (1.650-1.773; n = 242; P versus WT Canton-S > 0,05). The logEC50-value for sh(102) was 1.594 (1.493-1.694; n = 261; P versus sh(mns) > 0.05). The logEC-value of na[har(38)] was 2.076 (1.619-2.532; n = 207; P versus sh(mns) < 0.05, versus sh(102) < 0.05, versus WT Canton-S < 0.05). P values for all shaker mutants were P > 0.05, while na[har(38)] was found to be hyposensitive compared to wildtype (P < 0.05). CONCLUSIONS:The xenon requirement in Drosophila melanogaster is not influenced by a single gene mutation at the shaker locus, whereas a reduced expression of a nonselective cation channel leads to an increased xenon requirement. This supports the thesis that xenon mediates its effects not only via an antagonism at the NMDA-receptor.

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