Evidence map›Paper›PMID 9801355›Full record

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

A Ca2+/calmodulin-dependent protein kinase modulates Drosophila photoreceptor K+ currents: a role in shaping the photoreceptor potential.

A Peretz, I Abitbol, A Sobko, C F Wu, B Attali

Open access · bronzeAbstract read
In one paragraph

Article 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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cyclic nucleotide-induced bidirectional long-term synaptic plasticity inbioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Article
  7. The modulation of the excitability of primary sensory neurons by Ca²⁺-CaM-CaMKII pathway.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012
    Article
  8. Retrograde signaling from the brain to the retina modulates the termination of the light response in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  9. Article
  10. Article
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

5 authors at 2 institutions in 2 countries.

A PeretzNeurobiology Department, Weizmann Institute of Science, Rehovot 76100, Israel.
I Abitbol
A Sobko
C F Wu
B Attali
Weizmann Institute of Science · ILUniversity of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Light activation of Drosophila photoreceptors leads to the generation of a depolarizing receptor potential via opening of transient receptor potential and transient receptor potential-like cationic channels. Counteracting the light-activated depolarizing current are two voltage-gated K+ conductances, IA and IK, that are expressed in these sensory neurons. Here we show that Drosophila photoreceptors IA and IK are regulated by calcium-calmodulin (Ca2+/calmodulin) via a Ca2+/calmodulin-dependent protein kinase (CaM kinase), with IK being far more sensitive than IA. Inhibition of Ca2+/calmodulin by N-(6 aminohexyl)-5-chloro-1-naphthalenesulfonamide or trifluoperazine markedly reduced the K+ current amplitudes. Likewise, inhibition of CaM kinases by KN-93 potently depressed IK and accelerated its C-type inactivation kinetics. The effect of KN-93 was specific because its structurally related but functionally inactive analog KN-92 was totally ineffective. In Drosophila photoreceptor mutant ShKS133, which allows isolation of IK, we demonstrate by current-clamp recording that inhibition of IK by quinidine or tetraethylammonium increased the amplitude of the photoreceptor potential, depressed light adaptation, and slowed down the termination of the light response. Similar results were obtained when CaM kinases were blocked by KN-93. These findings place photoreceptor K+ channels as an additional target for Ca2+/calmodulin and suggest that IK is well suited to act in concert with other components of the signaling machinery to sharpen light response termination and fine tune photoreceptor sensitivity during light adaptation.

Indexed as

Adaptation, OcularAnimalsBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein KinasesDrosophilaDrosophila ProteinsEnzyme InhibitorsKineticsMembrane PotentialsPatch-Clamp TechniquesPhotoreceptor Cells, InvertebratePotassium ChannelsQuinidineReaction TimeShaker Superfamily of Potassium ChannelsBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein KinasesDrosophila ProteinsEnzyme InhibitorsKN 93Potassium ChannelsQuinidineShaker Superfamily of Potassium ChannelsSh protein, DrosophilaSulfonamidesTetraethylammoniumVasodilator AgentsW 7

Identifiers

PMID9801355
PMCPMC6792883
OpenAlexW2135654560

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.