ArticleJournal of pain research2026
Pharmacological Inhibition of Tropomyosin Receptor Kinase B Reverses Remifentanil-Induced Postoperative Hyperalgesia and Synaptic Remodeling.
Article in Journal of pain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors.
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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.
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