Evidence map›Paper›PMID 22952835›Full record

ArticlePloS one2012

Temporo-spectral imaging of intrinsic optical signals during hypoxia-induced spreading depression-like depolarization.

Maria Mané, Michael Müller

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Effect of hypoxia on BOLD fMRI response and total cerebral blood flow in migraine with aura patients.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Trial
  2. Article
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  7. Spreading depolarizations in the rat endothelin-1 model of focal cerebellar ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
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  8. Review
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  11. Large field-of-view movement-compensated intrinsic optical signal imaging for the characterization of the haemodynamic response to spreading depolarizations in large gyrencephalic brains.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  12. Heterogeneous incidence and propagation of spreading depolarizations.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
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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

2 authors at 1 institution in 1 country.

Maria ManéDFG Research Center Molecular Physiology of Brain, Zentrum für Physiologie und Pathophysiologie, Abteilung Neuro- und Sinnesphysiologie, Georg-August-Universität Göttingen, Göttingen, Germany.
Michael Müller
Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spreading depression (SD) is characterized by a sustained near-complete depolarization of neurons, a massive depolarization of glia, and a negative deflection of the extracellular DC potential. These electrophysiological signs are accompanied by an intrinsic optical signal (IOS) which arises from changes in light scattering and absorption. Even though the underlying mechanisms are unclear, the IOS serves as non-invasive tool to define the spatiotemporal dynamics of SD in brain slices. Usually the tissue is illuminated by white light, and light reflectance or transmittance is monitored. Using a polychromatic, fast-switchable light source we now performed temporo-spectral recordings of the IOS associated with hypoxia-induced SD-like depolarization (HSD) in rat hippocampal slices kept in an interface recording chamber. Recording full illumination spectra (320-680 nm) yielded distinct reflectance profiles for the different phases of HSD. Early during hypoxia tissue reflectance decreased within almost the entire spectrum due to cell swelling. HSD was accompanied by a reversible reflectance increase being most pronounced at 400 nm and 460 nm. At 440 nm massive porphyrin absorption (Soret band) was detected. Hypotonic solutions, Ca(2+)-withdrawal and glial poisoning intensified the reflectance increase during HSD, whereas hypertonic solutions dampened it. Replacement of Cl(-) inverted the reflectance increase. Inducing HSD by cyanide distorted the IOS and reflectance at 340-400 nm increased irreversibly. The pronounced changes at short wavelengths (380 nm, 460 nm) and their cyanide sensitivity suggest that block of mitochondrial metabolism contributes to the IOS during HSD. For stable and reliable IOS recordings during HSD wavelengths of 460-560 nm are recommended.

Indexed as

Cortical Spreading DepressionMembrane PotentialsOptical ImagingAnimalsCalciumHippocampusHypoxiaMaleMitochondriaNeurogliaNeuronsOsmolar ConcentrationRatsRats, Sprague-DawleyTime FactorsCalcium

Identifiers

PMID22952835
PMCPMC3430631
OpenAlexW2021555429

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.