Evidence map›Paper›PMID 25092243›Full record

ArticleMolecular psychiatry2015

Dentate gyrus-CA3 glutamate release/NMDA transmission mediates behavioral despair and antidepressant-like responses to leptin.

X Wang, D Zhang, X-Y Lu

Open access · greenAbstract read
In one paragraph

Article in Molecular psychiatry, 2015. 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
1.6field-weighted citation impact, top 21% 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, 43 citations in OpenAlex.

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  11. Oxidative medicine and cellular longevity · 2021
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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.

X Wang1] 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.
D ZhangDepartment of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
X-Y LuDepartment of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
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
Adiponectin regulation of the mesolimbic dopamine systemR21MH096251 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LODGE, DANIEL, LU, XIN-YUN · 2012 to 2013
$399k
NCATS NIH HHS UL1 TR001120NIMH NIH HHS MH076929NIMH NIH HHS MH100583NIMH NIH HHS R01 MH076929NIMH NIH HHS R01 MH100583NIMH NIH HHS R21 MH096251
6 · The paper itself

Abstract

Compelling evidence supports the important role of the glutamatergic system in the pathophysiology of major depression and also as a target for rapid-acting antidepressants. However, the functional role of glutamate release/transmission in behavioral processes related to depression and antidepressant efficacy remains to be elucidated. In this study, glutamate release and behavioral responses to tail suspension, a procedure commonly used for inducing behavioral despair, were simultaneously monitored in real time. The onset of tail suspension stress evoked a rapid increase in glutamate release in hippocampal field CA3, which declined gradually after its offset. Blockade of N-methyl-D-aspartic acid (NMDA) receptors by intra-CA3 infusion of MK-801, a non-competitive NMDA receptor antagonist, reversed behavioral despair. A subpopulation of granule neurons that innervated the CA3 region expressed leptin receptors and these cells were not activated by stress. Leptin treatment dampened tail suspension-evoked glutamate release in CA3. On the other hand, intra-CA3 infusion of NMDA blocked the antidepressant-like effect of leptin in reversing behavioral despair in both the tail suspension and forced swim tests, which involved activation of Akt signaling in DG. Taken together, these results suggest that the DG-CA3 glutamatergic pathway is critical for mediating behavioral despair and antidepressant-like responses to leptin.

Indexed as

AnimalsAntidepressive AgentsCA3 Region, HippocampalDentate GyrusDepressionDisease Models, AnimalEnzyme InhibitorsExcitatory Amino Acid AgentsGene Expression RegulationGlutamic AcidLeptinMaleMiceMice, Inbred C57BLMice, TransgenicMotor ActivityAntidepressive AgentsEnzyme InhibitorsExcitatory Amino Acid AgentsGlutamic AcidGt(ROSA)26Sor non-coding RNA, mouseLeptinN-MethylaspartateReceptors, LeptinRNA, Untranslated

Identifiers

PMID25092243
PMCPMC4362753
OpenAlexW1974206938

What OpenQuestion holds

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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.