Evidence map›Paper›PMID 25821602›Full record

ArticleNeural plasticity2015

Age-related alterations in the expression of genes and synaptic plasticity associated with nitric oxide signaling in the mouse dorsal striatum.

Aisa N Chepkova, Susanne Schönfeld, Olga A Sergeeva

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Intact corticostriatal function in aged system xTranslational psychiatry · 2025
    Article
  2. An Overview of NO Signaling Pathways in Aging.Molecules (Basel, Switzerland) · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. 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

3 authors at 1 institution in 1 country.

Aisa N ChepkovaDepartment of Molecular Neurophysiology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Susanne SchönfeldDepartment of Molecular Neurophysiology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Olga A SergeevaDepartment of Molecular Neurophysiology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related alterations in the expression of genes and corticostriatal synaptic plasticity were studied in the dorsal striatum of mice of four age groups from young (2-3 months old) to old (18-24 months of age) animals. A significant decrease in transcripts encoding neuronal nitric oxide (NO) synthase and receptors involved in its activation (NR1 subunit of the glutamate NMDA receptor and D1 dopamine receptor) was found in the striatum of old mice using gene array and real-time RT-PCR analysis. The old striatum showed also a significantly higher number of GFAP-expressing astrocytes and an increased expression of astroglial, inflammatory, and oxidative stress markers. Field potential recordings from striatal slices revealed age-related alterations in the magnitude and dynamics of electrically induced long-term depression (LTD) and significant enhancement of electrically induced long-term potentiation in the middle-aged striatum (6-7 and 12-13 months of age). Corticostriatal NO-dependent LTD induced by pharmacological activation of group I metabotropic glutamate receptors underwent significant reduction with aging and could be restored by inhibition of cGMP hydrolysis indicating that its age-related deficit is caused by an altered NO-cGMP signaling cascade. It is suggested that age-related alterations in corticostriatal synaptic plasticity may result from functional alterations in receptor-activated signaling cascades associated with increasing neuroinflammation and a prooxidant state.

Indexed as

Gene ExpressionAgingAnimalsAstrocytesGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsMaleMiceMice, TransgenicNeostriatumNerve Tissue ProteinsNeuronal PlasticityNitric OxideNitric Oxide SynthaseOxidative StressReceptors, Dopamine D1dopamine D1A receptorGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseGreen Fluorescent ProteinsNerve Tissue ProteinsNitric OxideNitric Oxide SynthaseNR1 NMDA receptorReceptors, Dopamine D1Receptors, N-Methyl-D-Aspartate

Identifiers

PMID25821602
PMCPMC4364378
OpenAlexW1994247466

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.