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Chronic morphine administration often leads to the development of antinociceptive tolerance, presenting a significant challenge in the chronic pain management. Although microglia are known to mediate the neuroinflammation associated with morphine-induced antinociceptive tolerance, the molecular mechanisms underlying this process remain incompletely understood. Recent evidence indicates that T cell immunoglobulin domain and mucin domain-3 (TIM3) acts as an important regulator in inflammation-related diseases. In this study, we investigated the role of TIM3 in morphine antinociceptive tolerance. Pharmacological blockade of TIM3 exacerbated morphine antinociceptive tolerance and associated hyperalgesia, whereas upregulation of TIM3 in the spinal cord significantly reduced both the development and maintenance of antinociceptive tolerance. We found that TIM3 negatively regulated microglia-mediated neuroinflammation and neuronal apoptosis following chronic morphine exposure. Mechanistically, TIM3 promoted the degradation of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibited the activation of nuclear factor κB (NF-κB) signaling pathways. Furthermore, we identified TRAF6 as a key mediator through which TIM3 attenuated morphine-induced antinociceptive tolerance and suppressed the secretion of proinflammatory factors. Notably, TIM3 interacted with tumor necrosis factor α-induced protein 3 (TNFAIP3) to enhance K48-linked ubiquitination of TRAF6 in morphine-stimulated microglia, thereby mitigating inflammatory responses. Together, these findings suggest that spinal TIM3 negatively modulates morphine antinociceptive tolerance by regulating microglial inflammatory responses through a TNFAIP3/TRAF6/NF-κB-dependent mechanism. This study highlights TIM3 as a promising therapeutic target for preventing morphine antinociceptive tolerance in chronic pain management. Schematic diagram for the proposed mechanisms of TIM3 regulates morphine antinociceptive tolerance. TIM3 may alleviate morphine antinociceptive tolerance by suppressing microglia-mediated neuroinflammation and neuronal apoptosis, which is associated with the TRAF6/NF-κB pathway.
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http://dx.doi.org/10.1016/j.neuropharm.2025.110638 | DOI Listing |
Neuropsychopharmacology
September 2025
School of Biological Sciences, Centre for Biodiscovery, Victoria University of Wellington, Wellington, 6012, New Zealand.
The development of safer mu opioid receptor (MOR) agonists with reduced side effects is a key focus of pain research. Some studies have suggested that MOR agonists with reduced β-arrestin 2 (βArr2) signaling (i.e.
View Article and Find Full Text PDFComput Biol Chem
August 2025
H. E. J. Research Institute of Chemistry, International Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan; Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi
Chronic pain is a maladaptive state where pain signals persist beyond the expected resolution of injury or illness. Morphine and related compounds, acting as µ-opioid receptor (µOR) agonists, are effective analgesics for managing this condition. However, chronic morphine administration can disrupt µOR trafficking and activate β-arrestin-mediated pathways, leading to opioid tolerance.
View Article and Find Full Text PDFAm J Vet Res
August 2025
KL Maddy Equine Analytical Chemistry Laboratory, Section of Pharmacology, School of Veterinary Medicine, University of California-Davis, Davis, CA.
Objective: To investigate the effect of cannabidiol (CBD) on thermal and mechanical thresholds and physiologic variables in horses.
Methods: 6 horses (3 geldings and 3 mares) were enrolled in a prospective, randomized, masked crossover design from March 18 through May 3, 2025. Horses received 3.
Br J Pharmacol
August 2025
Key Laboratory of Preclinical Study for New Drugs of Gansu Province and School of Basic Medical Sciences, Lanzhou University, Lanzhou, China.
Background And Purpose: The opioid crisis caused by the proliferation of fentanyl-related drugs has intensified concerns about the utilisation of opioid analgesics. Herein, a novel peptide-drug conjugate FENPFF01, incorporating the neuropeptide FF (NPFF) and fentanyl pharmacophores, was synthesised and pharmacologically characterised.
Experimental Approach: The agonist activities of FENPFF01 at opioid and NPFF receptors were characterised in in vitro functional assays.
Neuropharmacology
November 2025
Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical University, Xuzhou, Jiangsu, China. Electronic address:
Chronic morphine administration often leads to the development of antinociceptive tolerance, presenting a significant challenge in the chronic pain management. Although microglia are known to mediate the neuroinflammation associated with morphine-induced antinociceptive tolerance, the molecular mechanisms underlying this process remain incompletely understood. Recent evidence indicates that T cell immunoglobulin domain and mucin domain-3 (TIM3) acts as an important regulator in inflammation-related diseases.
View Article and Find Full Text PDF