Evidence map›Paper›PMID 9482810›Full record

ReviewThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

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

J E Engel, C F Wu

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 77 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Electrophysiological analysis of synaptic transmission in Drosophila.Wiley interdisciplinary reviews. Developmental biology · 2017
    Review
  6. BK Channels Mediate Synaptic Plasticity Underlying Habituation in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  7. Article
  8. Article
  9. The transcription factors islet and Lim3 combinatorially regulate ion channel gene expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  10. An evolutionarily conserved mode of modulation of Shaw-like K⁺ channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  11. Article
  12. Article
  13. Article
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  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

J E EngelDepartment of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA.
C F Wu
University of Iowa · US

Funding

Plasticity of Neuronal Function and Form in DrosophilaR01NS026528 · NINDS · UNIVERSITY OF IOWA · PI WU, CHUN-FANG · 1988 to 2007
$2.0M
PHYSIOLOGY OF EXCITABLE MEMBRANE AND SYNAPSER01NS018500 · NINDS · UNIVERSITY OF IOWA · PI WU, CHUN-FANG · 1985 to 2000
$239k
NINDS NIH HHS NS18500NINDS NIH HHS NS26528
6 · The paper itself

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.

Indexed as

AnimalsDrosophilaEscape ReactionHabituation, PsychophysiologicMutationNervous System Physiological PhenomenaPotassium ChannelsReaction TimeRefractory Period, ElectrophysiologicalPotassium Channels

Identifiers

PMID9482810
PMCPMC6792913
OpenAlexW2127263164

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.