Mutational and pharmacological alterations of neuronal membrane function disrupt conditioning in Drosophila.
Neuronal membrane channels of Drosophila melanogaster were altered either genetically or pharmacologically in order to investigate the role of specific ionic currents in the acquisition and retention of a conditioned behavior. Conditioning could not be detected for Shaker mutants, in which the fast transient potassium current (IA) is altered; a second potassium channel mutant, eag (ether a go-go) is conditioned like wild type, but the retention period is abnormally short. The napts mutant (no action potential, temperature sensitive), in which nerve excitability is reduced, also expresses normal acquisition and a shortened period of retention. Double mutants of Sh5 and napts as well as Sh5 treated with tetrodotoxin, are essentially normal with respect to acquisition; in both cases these flies remain retention-defective. These experiments therefore reveal a behavioral phenotype of Drosophila mutants in which the primary physiological defect seems to be in the functioning of specific neuronal ionic channels.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D003214:Conditioning, Classical / Q000187:drug effects*; D003380:Courtship; D004331:Drosophila melanogaster; D005260:Female; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D008297:Male; D009154:Mutation; D009431:Neural Conduction / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D010641:Phenotype; D011930:Reaction Time; D013696:Temperature; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D013779:Tetrodotoxin