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

doi:10.1523/jneurosci.18-22-09153.1998

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

Journal article

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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 and B Attali

The Journal of neuroscience, Vol.18(22), pp.9153-9162

11/15/1998

DOI: 10.1523/jneurosci.18-22-09153.1998

PMID: 9801355

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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.

Membrane Potentials - drug effects

Drosophila Proteins

Tetraethylammonium - pharmacology

Vasodilator Agents - pharmacology

Drosophila

Enzyme Inhibitors - pharmacology

Photoreceptor Cells, Invertebrate - enzymology

Quinidine - pharmacology

Reaction Time - physiology

Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors

Membrane Potentials - physiology

Sulfonamides - pharmacology

Potassium Channels - metabolism

Vision, Ocular - physiology

Patch-Clamp Techniques

Animals

Photoreceptor Cells, Invertebrate - chemistry

Adaptation, Ocular - physiology

Kinetics

Shaker Superfamily of Potassium Channels

Benzylamines - pharmacology

Calcium-Calmodulin-Dependent Protein Kinases - metabolism

Details

Title: Subtitle: A Ca2+/calmodulin-dependent protein kinase modulates Drosophila photoreceptor K+ currents: a role in shaping the photoreceptor potential
Creators: A Peretz - Neurobiology Department, Weizmann Institute of Science, Rehovot 76100, Israel
I Abitbol
A Sobko
C F Wu
B Attali
Resource Type: Journal article
Publication Details: The Journal of neuroscience, Vol.18(22), pp.9153-9162
DOI: 10.1523/jneurosci.18-22-09153.1998
PMID: 9801355
NLM abbreviation: J Neurosci
ISSN: 0270-6474
eISSN: 1529-2401
Publisher: United States
Language: English
Date published: 11/15/1998
Academic Unit: Iowa Neuroscience Institute; Biology
Record Identifier: 9984070356202771

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