OSCR

Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling.

Overview

Authors: Lijun Yang1, Yu Huang1, Bo Long2
ORCID iDs: Bo Long
  1. Department of Anesthesiology,Fujian Maternity and Child Health Hospital College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, 350001, People’s Republic of China
  2. Department of Anesthesiology,The Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, 350001, People’s Republic of China
Journal: Journal of pain research, volume 19, article 598801
Dates: received 27 January 2026; accepted 17 June 2026; published online 29 June 2026
Type: Research article · Language: English
License: CC BY-NC
Identifiers: DOI 10.2147/jpr.s598801 · PMID 42404688 · PMCID PMC13331029 · OpenAlex W7166558976
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: rat (organism), pain (population), cellular / molecular (subfield)
Methods: Statistics, Physiology & signal measures
Keywords: remifentanil, hyperalgesia, tropomyosin receptor kinase B, brain-derived neurotrophic factor, neuroplasticity
Topic: Pain Mechanisms and Treatments (Physiology, Medicine), according to OpenAlex
Funding: Joint Funds for the Innovation of Science and Technology, Fujian province
Citations: not cited yet (Europe PMC); 34 references in the paper

Abstract

Purpose: This study investigated the contributions of tropomyosin receptor kinase B (TrkB) signaling to behavioral hyperalgesia and associated spinal synaptic and dendritic remodeling in the rat remifentanil-induced hyperalgesia (RIH) model.

Methods: Forty rats were randomly assigned to four treatment groups (n = 10/group): normal saline + TrkB inhibitor (NS + ANA), surgical incision of the hind paw (I), remifentanil + incision (IR), and remifentanil + incision + TrkB inhibitor (IR + ANA). Paw mechanical withdrawal threshold (PMWT), expression levels of Brain-derived neurotrophic factor (BDNF), TrkB, and synaptic proteins, and dendritic morphology were compared among groups.

Results: Rats in the IR group exhibited significantly reduced mechanical pain thresholds and elevated expression levels of BDNF, TrkB, the glutamate receptor 1 subunit (GluR1), postsynaptic density protein 95 (PSD-95), and synapsin compared to the I group at 48 h post-surgery. In addition, IR rats had longer spinal dendrites with greater branching complexity. Administration of a TrkB inhibitor (IR + ANA group) reversed all these changes, with the exception of upregulated BDNF expression.

Conclusion: This study provides molecular and morphological evidence that TrkB inhibition reverses synaptic structural remodeling in RIH, suggesting TrkB as a potential therapeutic target. The feasibility of TrkB inhibitors for human postoperative hyperalgesia warrants further investigation.

Reproduced under the paper's license (CC BY-NC), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 3 authors, 5 keywords, 1 funder, 34 references.

Cite

This paper

Yang, L., Huang, Y., & Long, B. (2026). Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling. Journal of pain research, 19, 598801. https://doi.org/10.2147/jpr.s598801

BibTeX

@article{yang2026pharmacological,
author = {Yang, Lijun and Huang, Yu and Long, Bo},
title = {{Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling}},
journal = {Journal of pain research},
year = {2026},
month = jun,
volume = {19},
pages = {598801},
publisher = {Dove Press},
issn = {1178-7090},
doi = {10.2147/jpr.s598801},
url = {https://doi.org/10.2147/jpr.s598801},
pmid = {42404688},
pmcid = {PMC13331029}
}

RIS

TY - JOUR
AU - Yang, Lijun
AU - Huang, Yu
AU - Long, Bo
TI - Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling
T2 - Journal of pain research
J2 - J Pain Res
PY - 2026
DA - 2026/06/29
VL - 19
SP - 598801
SN - 1178-7090
PB - Dove Press
DO - 10.2147/jpr.s598801
UR - https://doi.org/10.2147/jpr.s598801
LA - en
ER -

CSL-JSON

{
"id": "10.2147/jpr.s598801",
"type": "article-journal",
"title": "Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling",
"container-title": "Journal of pain research",
"author": [
{
"family": "Yang",
"given": "Lijun"
},
{
"family": "Huang",
"given": "Yu"
},
{
"family": "Long",
"given": "Bo"
}
],
"container-title-short": "J Pain Res",
"volume": "19",
"page": "598801",
"DOI": "10.2147/jpr.s598801",
"PMID": "42404688",
"PMCID": "PMC13331029",
"ISSN": "1178-7090",
"publisher": "Dove Press",
"URL": "https://doi.org/10.2147/jpr.s598801",
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
29
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.3389/fphar.2026.1881525
Pentylenetetrazole kindling impairs place recognition memory associated with suppressing proBDNF-mediated neural information flows at the hippocampal CA3-CA1 synapses.
Journal: Frontiers in pharmacology
In common: rat, 1 reference
[2] doi:10.7554/elife.108845
Acute opioid responses are modulated by dynamic interactions of <i>Oprm1</i> and <i>Fgf12</i>.
Journal: eLife
In common: pain, rat, cellular / molecular
[3] doi:10.1172/jci197345
Catecholamine-mediated release of miR-133a-3p from adipocytes regulates the onset of chronic primary pain.
Journal: The Journal of clinical investigation
In common: pain, rat, cellular / molecular
[4] doi:10.1371/journal.pone.0351249
TNF-α exacerbates postoperative plantar pain by regulating the expression of Nav1.8.
Journal: PloS one
In common: pain, rat, cellular / molecular
[5] doi:10.1111/adb.70179 [code]
Transcriptional Response to Chronic Long-Access Fentanyl Self-Administration in Rat Habenula and Amygdala.
Journal: Addiction biology
In common: pain, rat, cellular / molecular
[6] doi:10.3390/cells15090775
Molecular Signatures of Maladaptive Plasticity in the Amygdala in a Rat Model of Chronic Neuropathic Pain.
Journal: Cells
In common: pain, rat, cellular / molecular
[7] doi:10.1172/jci.insight.202639
8-Aminoguanine protects against paclitaxel-induced neural degeneration and mechanical allodynia.
Journal: JCI insight
In common: pain, rat, cellular / molecular
[8] doi:10.1038/s41586-026-10299-9 [code]
A µ-opioid receptor superagonist analgesic with minimal adverse effects.
Journal: Nature
In common: pain, rat, cellular / molecular
[9] doi:10.1016/j.isci.2026.115629
Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice.
Journal: iScience
In common: 1 reference
[10] doi:10.1016/j.isci.2026.116152 [code]
Integrating multidimensional nociceptive-related cortical features for unsupervised assessment of anesthesia states in rats.
Journal: iScience
In common: pain, rat

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.