Evidence map›Paper›PMID 23936777›Full record

ArticleBioMed research international2013

Modulation of neurological deficits and expression of glutamate receptors during experimental autoimmune encephalomyelitis after treatment with selected antagonists of glutamate receptors.

Grzegorz Sulkowski, Beata Dąbrowska-Bouta, Lidia Strużyńska

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2013. 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 25% 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. Modulating glutamate neurotransmission inFrontiers in immunology · 2026
    Review
  2. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. CaMKIIα Mediates the Effect of IL-17 To Promote Ongoing Spontaneous and Evoked Pain in Multiple Sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  10. Glutamate, T cells and multiple sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2017
    Review
  11. Review
  12. 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

3 authors at 2 institutions in 1 country.

Grzegorz SulkowskiDepartment of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. gsulkowski@imdik.pan.pl
Beata Dąbrowska-Bouta
Lidia Strużyńska
Mossakowski Medical Research Institute, Polish Academy of Sciences · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of our investigation was to characterize the role of group I mGluRs and NMDA receptors in pathomechanisms of experimental autoimmune encephalomyelitis (EAE), the rodent model of MS. We tested the effects of LY 367385 (S-2-methyl-4-carboxyphenylglycine, a competitive antagonist of mGluR1), MPEP (2-methyl-6-(phenylethynyl)-pyridine, an antagonist of mGluR5), and the uncompetitive NMDA receptor antagonists amantadine and memantine on modulation of neurological deficits observed in rats with EAE. The neurological symptoms of EAE started at 10-11 days post-injection (d.p.i.) and peaked after 12-13 d.p.i. The protein levels of mGluRs and NMDA did not increase in early phases of EAE (4 d.p.i.), but starting from 8 d.p.i. to 25 d.p.i., we observed a significant elevation of mGluR1 and mGluR5 protein expression by about 20% and NMDA protein expression by about 10% over the control at 25 d.p.i. The changes in protein levels were accompanied by changes in mRNA expression of group I mGluRs and NMDARs. During the late disease phase (20-25 d.p.i.), the mRNA expression levels reached 300% of control values. In contrast, treatment with individual receptor antagonists resulted in a reduction of mRNA levels relative to untreated animals.

Indexed as

AmantadineAnimalsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalExcitatory Amino Acid AntagonistsFemaleGene Expression RegulationHumansHydrolasesMultiple SclerosisRatsReceptors, GlutamateReceptors, N-Methyl-D-AspartateRNA, MessengerAmantadineExcitatory Amino Acid AntagonistsHsaD protein, Mycobacterium tuberculosisHydrolasesReceptors, GlutamateReceptors, N-Methyl-D-AspartateRNA, Messenger

Identifiers

PMID23936777
PMCPMC3722774
OpenAlexW2146529272

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.