Evidence map›Paper›PMID 20410120›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Protein kinase G dynamically modulates TASK1-mediated leak K+ currents in cholinergic neurons of the basal forebrain.

Hiroki Toyoda, Mitsuru Saito, Makoto Okazawa, Keiko Hirao, Hajime Sato, Haruka Abe, Kenji Takada, Kazuo Funabiki, Masahiko Takada, Takeshi Kaneko and 1 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. TASK Channels on Basal Forebrain Cholinergic Neurons Modulate Electrocortical Signatures of Arousal by Histamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  10. Article
  11. Article
  12. Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
  13. 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

11 authors at 1 institution in 1 country.

Hiroki ToyodaDepartment of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan.
Mitsuru Saito
Makoto Okazawa
Keiko Hirao
Hajime Sato
Haruka Abe
Kenji Takada
Kazuo Funabiki
Masahiko Takada
Takeshi Kaneko
Youngnam Kang
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leak K(+) conductance generated by TASK1/3 channels is crucial for neuronal excitability. However, endogenous modulators activating TASK channels in neurons remained unknown. We previously reported that in the presumed cholinergic neurons of the basal forebrain (BF), activation of NO-cGMP-PKG (protein kinase G) pathway enhanced the TASK1-like leak K(+) current (I-K(leak)). As 8-Br-cGMP enhanced the I-K(leak) mainly at pH 7.3 as if changing the I-K(leak) from TASK1-like to TASK3-like current, such an enhancement of the I-K(leak) would result either from an enhancement of hidden TASK3 component or from an acidic shift in the pH sensitivity profile of TASK1 component. In view of the report that protonation of TASK channel decreases its open probability, the present study was designed to examine whether the activation of PKG increases the conductance of TASK1 channels by reducing their binding affinity for H(+), i.e., by increasing K(d) for protonation, or not. We here demonstrate that PKG activation and inhibition respectively upregulate and downregulate TASK1 channels heterologously expressed in PKG-loaded HEK293 cells at physiological pH, by causing shifts in the K(d) in the acidic and basic directions, respectively. Such PKG modulations of TASK1 channels were largely abolished by mutating pH sensor H98. In the BF neurons that were identified to express ChAT and TASK1 channels, similar dynamic modulations of TASK1-like pH sensitivity of I-K(leak) were caused by PKG. It is strongly suggested that PKG activation and inhibition dynamically modulate TASK1 currents at physiological pH by bidirectionally changing K(d) values for protonation of the extracellular pH sensors of TASK1 channels in cholinergic BF neurons.

Indexed as

Action PotentialsAnimalsCell LineCholinergic FibersCyclic GMP-Dependent Protein KinasesDown-RegulationFemaleHumansMaleMiceNerve Tissue ProteinsPotassium Channels, Tandem Pore DomainProsencephalonRatsRats, WistarUp-RegulationCyclic GMP-Dependent Protein KinasesNerve Tissue ProteinsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3

Identifiers

PMID20410120
PMCPMC6632358
OpenAlexW2062022185

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.