Evidence map›Paper›PMID 27917616›Full record

ArticleCNS neuroscience & therapeutics2017

Effect of Redox-Modifying Agents on the Activity of Channelrhodopsin-2.

Bao-Ming Wu, Tian-Dong Leng, Koichi Inoue, Jun Li, Zhi-Gang Xiong

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Arbitrary CaFrontiers in pharmacology · 2022
    Article
  2. 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 3 institutions in 3 countries.

Bao-Ming WuSchool of Pharmacy, Anhui Medical University, Hefei, China.
Tian-Dong LengNeuroscience Institute, Morehouse School of Medicine, Atlanta, GA, USA.
Koichi InoueDepartment of Integrative Anatomy, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Jun LiSchool of Pharmacy, Anhui Medical University, Hefei, China.
Zhi-Gang XiongSchool of Pharmacy, Anhui Medical University, Hefei, China.
Anhui Medical University · CNMorehouse School of Medicine · USNagoya City University · JP

Funding

Morehouse School of Medicine Center of Excellence Research Endowment ProgramS21MD000101 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI MONTGOMERY-RICE, VALERIE C. · 2001 to 2015
$74.3M
Program Evaluation - Internal & External U54NS083932 · NINDS · MOREHOUSE SCHOOL OF MEDICINE · PI MACLEISH, PETER RAYMOND · 2013 to 2017
$7.7M
ASICs and increased ischemic brain injury in diabetic conditionR01NS066027 · NINDS · MOREHOUSE SCHOOL OF MEDICINE · PI XIONG, ZHIGANG · 2011 to 2015
$1.6M
NIMHD NIH HHS S21 MD000101NINDS NIH HHS R01 NS066027NINDS NIH HHS U54 NS083932
6 · The paper itself

Abstract

backgroundThe algal protein Channelrhodopsin-2 (ChR2) has been widely used in recent years in optogenetic technique to investigate the functions of complex neuronal networks through minimally invasive and temporally precise photostimulation of genetically defined neurons. However, as with any other new technique, current optogentic approaches have various limitations. In addition, how ChR2 may behave in response to complex biochemical changes associated with various physiological/pathological conditions is largely unknown.

aimIn this study, we investigated whether a change in redox state of the cell affects the activity of ChR2 channels.

methodsWhole-cell patch-clamp recordings were used to examine the effect of reducing and oxidizing agents on ChR2 currents activated by blue light.

resultsWe show that the reducing agent dithiothreitol (DTT) dramatically potentiates the ChR2 currents in a reversible and concentration-dependent manner. Glutathione, an endogenous reducing agent, shows a similar effect on ChR2 currents. The oxidizing agent 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB) has no effect on ChR2 currents by itself; however, it completely reverses the potentiating effect of DTT. DTT also causes a shift in the current-voltage relationship by 23 ± 4.31 mV, suggesting a change in ion selectivity.

conclusionTaken together, these data suggest that redox modification of ChR2 plays an important role in its sensitivity to the light stimulation. Our findings not only help for a better understanding of how ChR2 may behave in physiological/pathological conditions where changes in redox state are common, but also provide a new direction for further optimization of this important opsin.

Indexed as

AnimalsBiophysicsChannelrhodopsinsCHO CellsCricetulusDithionitrobenzoic AcidDithiothreitolDose-Response Relationship, DrugElectric StimulationGlutathioneLightMembrane PotentialsOxidation-ReductionPatch-Clamp TechniquesReducing AgentsTransfectionChannelrhodopsinsDithionitrobenzoic AcidDithiothreitolGlutathioneReducing AgentsChR2DTTGSHOptogeneticsRedox reagents

Identifiers

PMID27917616
PMCPMC5310992
OpenAlexW2557774816

What OpenQuestion holds

Textmetadata
LicenceTDM
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.