Evidence map›Paper›PMID 22910678›Full record

ReviewNeuroscience and biobehavioral reviews2012

α2 adrenergic receptor dysregulation in depressive disorders: implications for the neurobiology of depression and antidepressant therapy.

Christopher Cottingham, Qin Wang

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 118 citations in OpenAlex.

  1. Evaluating the causal effects of circulating metabolites on major depression disorder.European archives of psychiatry and clinical neuroscience · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
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  9. Review
  10. Article
  11. LC-derived excitatory synaptic transmission to dorsal raphe serotonin neurons is inhibited by activation of alpha2-adrenergic receptors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  12. Review
  13. Review
  14. PET imaging of animal models with depressive-like phenotypes.European journal of nuclear medicine and molecular imaging · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Christopher CottinghamDepartment of Cell, Developmental & Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Qin Wang
University of Alabama at Birmingham · US

Funding

UAB Research Training Program in Neurobiology of Cognition and Cognitive DisordersT32NS061788 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Farah Dominique Lubin · 2008 to 2026
$4.5M
Regulation of novel alpha2A adrenergic receptor signaling by spinophilinR01MH081917 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2009 to 2019
$3.9M
NIMH NIH HHS MH081917NIMH NIH HHS R01 MH081917NINDS NIH HHS T32 NS061788NINDS NIH HHS T32 NS061788-03
6 · The paper itself

Abstract

Dysfunction in noradrenergic neurotransmission has long been theorized to occur in depressive disorders. The α2 adrenergic receptor (AR) family, as a group of key players in regulating the noradrenergic system, has been investigated for involvement in the neurobiology of depression and mechanisms of antidepressant therapies. However, a clear picture of the α2ARs in depressive disorders has not been established due to the existence of apparently conflicting findings in the literature. In this article, we report that a careful accounting of methodological differences within the literature can resolve the present lack of consensus on involvement of α2ARs in depression. In particular, the pharmacological properties of the radioligand (e.g. agonist versus antagonist) utilized for determining receptor density are crucial in determining study outcome. Upregulation of α2AR density detected by radiolabeled agonists but not by antagonists in patients with depressive disorders suggests a selective increase in the density of high-affinity conformational state α2ARs, which is indicative of enhanced G protein coupling to the receptor. Importantly, this high-affinity state α2AR upregulation can be normalized with antidepressant treatments. Thus, depressive disorders appear to be associated with increased α2AR sensitivity and responsiveness, which may represent a physiological basis for the putative noradrenergic dysfunction in depressive disorders. In addition, we review changes in some key α2AR accessory proteins in depressive disorders and discuss their potential contribution to α2AR dysfunction.

Indexed as

AnimalsAntidepressive AgentsDepressive DisorderGene Expression RegulationHumansModels, BiologicalNeurobiologyReceptors, Adrenergic, alpha-2Antidepressive AgentsReceptors, Adrenergic, alpha-2

Identifiers

PMID22910678
PMCPMC3508310
OpenAlexW2053624500

What OpenQuestion holds

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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.