Evidence map›Paper›PMID 36841465›Full record

ArticleExperimental neurology2023

Inhibition of monoamine oxidase-a increases respiration in isolated mouse cortical mitochondria.

Olivia J Kalimon, Hemendra J Vekaria, Greg A Gerhardt, Patrick G Sullivan

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
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

4 authors at 1 institution in 1 country.

Olivia J KalimonSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40356, USA; Department of Neuroscience, University of Kentucky, Lexington, KY 40508, USA; Lexington VA Healthcare System, Lexington, KY 40502, USA.
Hemendra J VekariaSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40356, USA; Department of Neuroscience, University of Kentucky, Lexington, KY 40508, USA; Lexington VA Healthcare System, Lexington, KY 40502, USA.
Greg A GerhardtSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40356, USA; Department of Neuroscience, University of Kentucky, Lexington, KY 40508, USA.
Patrick G SullivanSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40356, USA; Department of Neuroscience, University of Kentucky, Lexington, KY 40508, USA; Lexington VA Healthcare System, Lexington, KY 40502, USA. Electronic address: patsullivan@uky.edu.
University of Kentucky · US

Funding

Neurobiology of CNS Injury and RepairT32NS077889 · NINDS · UNIVERSITY OF KENTUCKY · PI Warren Joseph Alilain, JOHN C GENSEL · 2012 to 2026
$2.4M
NINDS NIH HHS T32 NS077889
6 · The paper itself

Abstract

Monoamine oxidase (MAO) is an enzyme located on the outer mitochondrial membrane that metabolizes amine substrates like serotonin, norepinephrine and dopamine. MAO inhibitors (MAOIs) are frequently utilized to treat disorders such as major depression or Parkinson's disease (PD), though their effects on brain mitochondrial bioenergetics are unclear. These studies measured bioenergetic activity in mitochondria isolated from the mouse cortex in the presence of inhibitors of either MAO-A, MAO-B, or both isoforms. We found that only 10 μM clorgyline, the selective inhibitor of MAO-A and not MAO-B, increased mitochondrial oxygen consumption rate in State V(CI) respiration compared to vehicle treatment. We then assessed mitochondrial bioenergetics, reactive oxygen species (ROS) production, and Electron Transport Chain (ETC) complex function in the presence of 0, 5, 10, 20, 40, or 80 μM of clorgyline to determine if this change was dose-dependent. The results showed increased oxygen consumption rates across the majority of respiration states in mitochondria treated with 5, 10, or 20 μM with significant bioenergetic inhibition at 80 μM clorgyline. Next, we assessed mitochondrial ROS production in the presence of the same concentrations of clorgyline in two different states: high mitochondrial membrane potential (ΔΨ

Indexed as

Monoamine OxidaseMonoamine Oxidase InhibitorsAnimalsCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneClorgylineMiceMitochondriaReactive Oxygen SpeciesRespirationCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneClorgylineMonoamine OxidaseMonoamine Oxidase InhibitorsReactive Oxygen SpeciesBioenergeticsClorgylineReactive oxygen species

Identifiers

PMID36841465
PMCPMC10073304
OpenAlexW4321793996

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.