Evidence map›Paper›PMID 26260133›Full record

ArticleMolecular brain2015

Persistent pain alters AMPA receptor subunit levels in the nucleus accumbens.

Chen Su, James D'amour, Michelle Lee, Hau-Yeuh Lin, Toby Manders, Duo Xu, Sarah E Eberle, Yossef Goffer, Anthony H Zou, Maisha Rahman and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 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
2.2field-weighted citation impact, top 13% 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, 45 citations in OpenAlex.

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  9. The mechanisms and management of persistent postsurgical pain.Frontiers in pain research (Lausanne, Switzerland) · 2023
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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

14 authors at 2 institutions in 2 countries.

Chen SuDepartment of Anesthesiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China. su.chen@nyumc.org.
James D'amourDepartments of Otolaryngology and Physiology and Neuroscience, The Helen and Martin Kimmel Center for Biology and Medicine at the Skirball Institute for Biomolecular Medicine, New York University School of Medicine, New York, NY, USA. James.D'Amour@med.nyu.edu.
Michelle LeeDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. michelle.lee022@gmail.com.
Hau-Yeuh LinDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. hauyuehlin@gmail.com.
Toby MandersDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. trm2124@gmail.com.
Duo XuDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. Duo.Xu@med.nyu.edu.
Sarah E EberleDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. sarah.e.eberle@gmail.com.
Yossef GofferDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. yg2149@gmail.com.
Anthony H ZouDepartment of Anesthesiology, New York University School of Medicine, New York, NY, USA. tonyhzou@gmail.com.
Maisha RahmanColumbia College, New York, NY, USA. maishyx16@gmail.com.
Edward ZiffDepartment of Biochemistry, New York University School of Medicine, New York, NY, USA. edward.ziff@nyumc.org.
Robert C FroemkeDepartments of Otolaryngology and Physiology and Neuroscience, The Helen and Martin Kimmel Center for Biology and Medicine at the Skirball Institute for Biomolecular Medicine, New York University School of Medicine, New York, NY, USA. Robert.Froemke@med.nyu.edu.
Dong HuangDepartment of Anesthesiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China. huangdong6619@vip.163.com.
Jing WangDepartments of Anesthesiology, Neuroscience and Physiology, New York University School of Medicine, New York, NY, USA. Jing.wang2@nyumc.org.
New York University · USCentral South University · CN

Funding

Central glutamate signaling in postoperative pain regulation - Revision - 1R01GM115384 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jing Wang · 2015 to 2026
$5.4M
Calcium Permeable AMPA Receptors: Signaling, Toxicity and ControlR01NS061920 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZIFF, EDWARD B · 2009 to 2013
$1.9M
CRCN: Dissecting Neural Circuits for Acute PainR01NS100065 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CHEN, ZHE SAGE, WANG, JING · 2016 to 2019
$1.5M
Postoperative pain increases synaptic GluA1 expression in the nucleus accumbens tK08GM102691 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WANG, JING · 2012 to 2015
$597k
NIGMS NIH HHS K08 GM102691NIGMS NIH HHS K08GM102691NIGMS NIH HHS R01 GM115384NIGMS NIH HHS R01GM115384NINDS NIH HHS R01 NS061920NINDS NIH HHS R01NS061920NINDS NIH HHS R01 NS100065
6 · The paper itself

Abstract

backgroundA variety of pain conditions have been found to be associated with depressed mood in clinical studies. Depression-like behaviors have also been described in animal models of persistent or chronic pain. In rodent chronic neuropathic pain models, elevated levels of GluA1 subunits of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the nucleus accumbens (NAc) have been found to inhibit depressive symptoms. However, the effect of reversible post-surgical pain or inflammatory pain on affective behaviors such as depression has not been well characterized in animal models. Neither is it known what time frame is required to elicit AMPA receptor subunit changes in the NAc in various pain conditions.

resultsIn this study, we compared behavioral and biochemical changes in three pain models: the paw incision (PI) model for post-incisional pain, the Complete Freund's Adjuvant (CFA) model for persistent but reversible inflammatory pain, and the spared nerve injury (SNI) model for chronic postoperative neuropathic pain. In all three models, rats developed depressive symptoms that were concurrent with the presentation of sensory allodynia. GluA1 levels at the synapses of the NAc, however, differed in these three models. The level of GluA1 subunits of AMPA-type receptors at NAc synapses was not altered in the PI model. GluA1 levels were elevated in the CFA model after a period (7 d) of persistent pain, leading to the formation of GluA2-lacking AMPA receptors. As pain symptoms began to resolve, however, GluA1 levels returned to baseline. Meanwhile, in the SNI model, in which pain persisted beyond 14 days, GluA1 levels began to rise after pain became persistent and remained elevated. In addition, we found that blocking GluA2-lacking AMPA receptors in the NAc further decreased the depressive symptoms only in persistent pain models.

conclusionOur study shows that while both short-term and persistent pain can trigger depression-like behaviors, GluA1 upregulation in the NAc likely represents a unique adaptive response to minimize depressive symptoms in persistent pain states.

Indexed as

AnimalsBehavior, AnimalChronic PainDepressionFreund's AdjuvantInflammationMaleNeuralgiaNucleus AccumbensProtein SubunitsProtein TransportRatsRats, Sprague-DawleyReceptors, AMPASynapsesFreund's AdjuvantProtein SubunitsReceptors, AMPA

Identifiers

PMID26260133
PMCPMC4531890
OpenAlexW2141415790

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.