Evidence map›Paper›PMID 25463972›Full record

ArticleTranslational psychiatry2014

Leptin receptor deficiency confers resistance to behavioral effects of fluoxetine and desipramine via separable substrates.

M Guo, X-Y Lu

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-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

30 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Interactive Effects of Serum Leptin Levels and Physical Comorbidity on the Pharmacotherapeutic Response of Depressive Disorders.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Systemic TNF-α blockade attenuates anxiety and depressive-like behaviors inSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Leptin Increases Expression of 5-HTFrontiers in psychiatry · 2018
    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.

M Guo1] Institute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China [2] Department of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
X-Y Lu1] Institute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China [2] Department of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Binzhou University · CN

Funding

Characterization of leptin's antidepressant activityR01MH076929 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LU, XIN-YUN · 2007 to 2016
$3.3M
Adiponectin signaling in mood regulationR01MH100583 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LU, XIN-YUN · 2013 to 2017
$1.9M
NIMH NIH HHS R01 MH076929NIMH NIH HHS R01 MH100583
6 · The paper itself

Abstract

Depression is a complex, heterogeneous mental disorder. Currently available antidepressants are only effective in about one-third to one-half of all patients. The mechanisms underlying antidepressant response and treatment resistance are poorly understood. Recent clinical evidence implicates the involvement of leptin in treatment response to antidepressants. In this study, we determined the functional role of the leptin receptor (LepRb) in behavioral responses to the selective serotonergic antidepressant fluoxetine and the noradrenergic antidepressant desipramine. While acute and chronic treatment with fluoxetine or desipramine in wild-type mice elicited antidepressant-like effects in the forced swim test, mice null for LepRb (db/db) displayed resistance to treatment with either fluoxetine or desipramine. Fluoxetine stimulated phosphorylation of Akt(Thr308) and GSK-3β(Ser9) in the hippocampus and prefrontal cortex (PFC) of wild-type mice but not in db/db mice. Desipramine failed to induce measurable changes in Akt, GSK-3β or ERK1/2 phosphorylation in the hippocampus and PFC, as well as hypothalamus of either genotype of mice. Deletion of LepRb specifically from hippocampal and cortical neurons resulted in fluoxetine insensitivity in the forced swim test and tail suspension test while leaving the response to desipramine intact. These results suggest that functional LepRb is critically involved in regulating the antidepressant-like behavioral effects of both fluoxetine and desipramine. The antidepressant effects of fluoxetine but not desipramine are dependent on the presence of functional LepRb in the hippocampus and cortex.

Indexed as

Adrenergic Uptake InhibitorsAnimalsBehavior, AnimalDepressive Disorder, Treatment-ResistantDesipramineFluoxetineHippocampusHypothalamusMiceMice, KnockoutPrefrontal CortexReceptors, LeptinSelective Serotonin Reuptake InhibitorsSignal TransductionAdrenergic Uptake InhibitorsDesipramineFluoxetineleptin receptor, mouseReceptors, LeptinSelective Serotonin Reuptake Inhibitors

Identifiers

PMID25463972
PMCPMC4270309
OpenAlexW2025875119

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.