Evidence map›Paper›PMID 17915260›Full record

ArticleLife sciences2007

Nitric oxide signaling participates in norepinephrine-induced activity of neuronal intracellular survival pathways.

Michael J Chen, Amelia A Russo-Neustadt

Open access · greenAbstract read
In one paragraph

Article in Life sciences, 2007. 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 28% 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, 38 citations in OpenAlex.

  1. Article
  2. Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Physical activity, air pollution and the brain.Sports medicine (Auckland, N.Z.) · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

Michael J ChenDepartment of Biological Sciences, California State University, 5151 State University Drive, Los Angeles, CA 90032, USA. mjchen@calstatela.edu
Amelia A Russo-Neustadt
California State University Los Angeles · US

Funding

PHYSICAL ACTIVITY, ANTIDEPRESSENTS AND BDNF INDUCTIONR01MH059776 · NIMH · UNIVERSITY OF CALIFORNIA IRVINE · PI RUSSO-NEUSTADT, AMELIA A · 1999 to 2008
$2.1M
NIMH NIH HHS MH 59776NIMH NIH HHS R01 MH059776
6 · The paper itself

Abstract

Much evidence has gathered that nitric oxide (NO) signaling, via cGMP-dependent mechanisms, may activate pro-survival pathways in hippocampal neurons and inhibit apoptosis. Past research has revealed that the enhancement of monoaminergic neurotransmission via exercise or treatment with antidepressant medications leads to an enhanced expression of brain-derived neurotrophic factor (BDNF). In isolated hippocampal neurons, norepinephrine (NE) application also increases the immunoreactivity of BDNF and several pro-survival signaling molecules. The data herein support the possibility that NO signaling plays an important role in enhancing neurotrophin expression and activation of the pro-survival phosphatidylinositol 3' kinase (PI-3K) pathway stimulated by NE. In isolated hippocampal neurons, the NO donor, sodium nitroprusside, increases BDNF, PI-3K, and phospho-ERK1 immunoreactivity. Specific inhibitors of the NO system suggest that NE-induced increases in hippocampal BDNF and the PI-3K pathway, but not stimulation of the MAPK pathway, depend upon NO signaling. In addition, inhibiting cGMP suggest that the effects of NE on BDNF immunoreactivity and Akt phosphorylation are also cGMP-dependent. Finally, the application of l-NAME to hippocampal neurons increases cell death. This is the first study of its kind demonstrating the involvement of NE-induced pro-survival signaling in three distinct signaling pathways: PI-3K, MAPK, and NO/cGMP. Possible mechanisms are discussed in light of the results.

Indexed as

HippocampusNeuronsAnimalsBlotting, WesternBrain-Derived Neurotrophic FactorCells, CulturedCell SurvivalCyclic GMPElectrophoresis, Polyacrylamide GelEnzyme InhibitorsFemaleGestational AgeGuanylate CyclaseMitogen-Activated Protein Kinase KinasesNitric OxideNitric Oxide DonorsBrain-Derived Neurotrophic FactorCyclic GMPEnzyme InhibitorsGuanylate CyclaseMitogen-Activated Protein Kinase KinasesNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNorepinephrinePhosphatidylinositol 3-Kinases

Identifiers

PMID17915260
PMCPMC2435382
OpenAlexW2021905491

What OpenQuestion holds

Textmetadata
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.