This laboratory has reported that some mutations in genes that encode ion channels influence the sensitivity of Drosophila to volatile general anesthetics in behavioral assays. In our present study we use electrophysiological recording from flight and jump muscles to monitor the response of a particular neural pathway when different stimulating voltages are applied across the eyes to the brain. We find that the more distal part of the pathway (from a giant fiber neuron through one or two interneurons to muscle), is very insensitive to halothane. However, synaptic transmission in the fly brain upstream of the giant fiber, represented by a long latency response to stimulating voltage, is inhibited by clinical doses of halothane. When Sh and eag mutants are assayed, there is a good correlation between the published effect of the mutations on the peak amplitude of the A-type current in larval muscle and their effect on halothane sensitivity of the long latency response. Genetic tests that the phenotype of these strains is due to the corresponding mutation in the potassium channel genes. These results indicate that the A-type K+ channel in CNS is a target for general anesthetics or at least influences a cell containing the target. Another mutation that shows strong behavioral and electrophysiological effects, har38, has not yet been characterized in detail. Genetic manipulation of this mutant has been expedited by showing that a change in abdominal morphology is associated with it.
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