Evidence map›Paper›PMID 30028316›Full record

ReviewNeural regeneration research2018

Molecular mechanism of noradrenaline during the stress-induced major depressive disorder.

Kenjiro Seki, Satomi Yoshida, Manoj Kumar Jaiswal

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Pathophysiology and Treatment Strategies for Different Types of Depression.Advances in experimental medicine and biology · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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 2 countries.

Kenjiro SekiDepartment of Pharmacology, School of Pharmaceutical Science, Ohu University, Fukushima, Japan.
Satomi YoshidaDepartment of Pharmacology, School of Pharmaceutical Science, Ohu University, Fukushima, Japan.
Manoj Kumar JaiswalDepartment of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Ohu University · JPIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic stress-induced depression is a common hallmark of many psychiatric disorders with high morbidity rate. Stress-induced dysregulation of noradrenergic system has been implicated in the pathogenesis of depression. Lack of monoamine in the brain has been believed to be the main causative factor behind pathophysiology of major depressive disorder (MDD) and several antidepressants functions by increasing the monoamine level at the synapses in the brain. However, it is undetermined whether the noradrenergic receptor stimulation is critical for the therapeutic effect of antidepressant. Contrary to noradrenergic receptor stimulation, it has been suggested that the desensitization of β-adrenoceptor is involved in the therapeutic effect of antidepressant. In addition, enhanced noradrenaline (NA) release is central response to stress and thought to be a risk factor for the development of MDD. Moreover, fast acting antidepressant suppresses the hyperactivation of noradrenergic neurons in locus coeruleus (LC). However, it is unclear how they alter the firing activity of LC neurons. These inconsistent reports about antidepressant effect of NA-reuptake inhibitors (NRIs) and enhanced release of NA as a stress response complicate our understanding about the pathophysiology of MDD. In this review, we will discuss the role of NA in pathophysiology of stress and the mechanism of therapeutic effect of NA in MDD. We will also discuss the possible contributions of each subtype of noradrenergic receptors on LC neurons, hypothalamic-pituitary-adrenal axis (HPA-axis) and brain derived neurotrophic factor-induced hippocampal neurogenesis during stress and therapeutic effect of NRIs in MDD.

Indexed as

hypothalamic-pituitary-adrenal axislocus coeruleusmajor depressionnoradrenalinenoradrenaline-reuptake inhibitorsselective serotonin reuptake inhibitorsserotonin noradrenaline-reuptake inhibitorsserotonin receptorsstress

Identifiers

PMID30028316
PMCPMC6065220
OpenAlexW2884197960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.