The Shaker Potassium Channel Is No Target for Xenon Anesthesia in Short-Sleeping Drosophila melanogaster Mutants

Abstract EN

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[har38].

Methods.

The Drosophila melanogaster strains wildtype Canton-S, na[har38], sh102 and shmns, 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 sh102 > 0,05), for shmns 1.711 (1.650–1.773; n=242; P versus WT Canton-S > 0,05).

The logEC50-value for sh102 was 1.594 (1.493–1.694; n=261; P versus shmns > 0.05).

The logEC-value of na[har38] was 2.076 (1.619–2.532; n=207; P versus shmns < 0.05, versus sh102 < 0.05, versus WT Canton-S < 0.05).

P values for all shaker mutants were P>0.05, while na[har38] 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.