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Genetic dissection of functional contributions of specific potassium channel subunits in habituation of an escape circuit in Drosophila
Journal article   Open access   Peer reviewed

Genetic dissection of functional contributions of specific potassium channel subunits in habituation of an escape circuit in Drosophila

J E Engel and C F Wu
The Journal of neuroscience, Vol.18(6), pp.2254-2267
03/15/1998
DOI: 10.1523/jneurosci.18-06-02254.1998
PMID: 9482810
url
https://doi.org/10.1523/jneurosci.18-06-02254.1998View
Published (Version of record) Open Access

Abstract

Potassium channels have been implicated in central roles in activity-dependent neural plasticity. The giant fiber escape pathway of Drosophila has been established as a model for analyzing habituation and its modification by memory mutations in an identified circuit. Several genes in Drosophila encoding K+ channel subunits have been characterized, permitting examination of the contributions of specific channel subunits to simple conditioning in an identified circuit that is amenable to genetic analysis. Our results show that mutations altering each of four K+ channel subunits (Sh, slo, eag, and Hk) have distinct effects on habituation at least as strong as those of dunce and rutabaga, memory mutants with defective cAMP metabolism (). Habituation, spontaneous recovery, and dishabituation of the electrically stimulated long-latency giant fiber pathway response were shown in each mutant type. Mutations of Sh (voltage-gated) and slo (Ca2+-gated) subunits enhanced and slowed habituation, respectively. However, mutations of eag and Hk subunits, which confer K+-current modulation, had even more extreme phenotypes, again enhancing and slowing habituation, respectively. In double mutants, Sh mutations moderated the strong phenotypes of eag and Hk, suggesting that their modulatory functions are best expressed in the presence of intact Sh subunits. Nonactivity-dependent responses (refractory period and latency) at two stages of the circuit were altered only in some mutants and do not account for modifications of habituation. Furthermore, failures of the long-latency response during habituation, which normally occur in labile connections in the brain, could be induced in the thoracic circuit stage in Hk mutants. Our work indicates that different K+ channel subunits play distinct roles in activity-dependent neural plasticity and thus can be incorporated along with second messenger "memory" loci to enrich the genetic analysis of learning and memory.
 Animals Refractory Period, Electrophysiological - physiology Habituation, Psychophysiologic - physiology Nervous System Physiological Phenomena Potassium Channels - physiology Mutation Reaction Time - physiology Escape Reaction - physiology Drosophila - physiology Drosophila - genetics Potassium Channels - genetics

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