scholarly journals μ‐Opioid receptors in primary sensory neurons are essential for opioid analgesic effect on acute and inflammatory pain and opioid‐induced hyperalgesia

2019 ◽  
Vol 597 (6) ◽  
pp. 1661-1675 ◽  
Author(s):  
Jie Sun ◽  
Shao‐Rui Chen ◽  
Hong Chen ◽  
Hui‐Lin Pan
Keyword(s):  
Sensory Neurons ◽  
Opioid Receptors ◽  
Inflammatory Pain ◽  
Analgesic Effect ◽  
Opioid Analgesic ◽  
Primary Sensory Neurons ◽  
Opioid Induced Hyperalgesia ◽  
Μ Opioid Receptors

scholarly journals Oligomerization of MrgC11 and μ-opioid receptors in sensory neurons enhances morphine analgesia

2018 ◽  
Vol 11 (535) ◽  
pp. eaao3134 ◽  
Author(s):  
Shao-Qiu He ◽  
Qian Xu ◽  
Vinod Tiwari ◽  
Fei Yang ◽  
Michael Anderson ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Opioid Receptors ◽  
Morphine Analgesia ◽  
Μ Opioid Receptors

scholarly journals Resolvin E1 Inhibits Substance P-Induced Potentiation of TRPV1 in Primary Sensory Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Youn Yi Jo ◽  
Ji Yeon Lee ◽  
Chul-Kyu Park
Keyword(s):  
Substance P ◽  
G Protein ◽  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Dorsal Root Ganglion Neurons ◽  
Peripheral Inflammation ◽  
Transient Receptor Potential Vanilloid ◽  
Primary Sensory Neurons ◽  
Nociceptive Neurons ◽  
Ganglion Neurons

The neuropeptide substance P (SP) is expressed in primary sensory neurons and is commonly regarded as a “pain” neurotransmitter. Upon peripheral inflammation, SP activates the neurokinin-1 (NK-1) receptor and potentiates activity of transient receptor potential vanilloid subtype 1 (TRPV1), which is coexpressed by nociceptive neurons. Therefore, SP functions as an important neurotransmitter involved in the hypersensitization of inflammatory pain. Resolvin E1 (RvE1), derived from omega-3 polyunsaturated fatty acids, inhibits TRPV1 activity via activation of the chemerin 23 receptor (ChemR23)—an RvE1 receptor located in dorsal root ganglion neurons—and therefore exerts an inhibitory effect on inflammatory pain. We demonstrate here that RvE1 regulates the SP-induced potentiation of TRPV1 via G-protein coupled receptor (GPCR) on peripheral nociceptive neurons. SP-induced potentiation of TRPV1 inhibited by RvE1 was blocked by the Gαi-coupled GPCR inhibitor pertussis toxin and the G-protein inhibitor GDPβ-S. These results indicate that a low concentration of RvE1 strongly inhibits the potentiation of TRPV1, induced by the SP-mediated activation of NK-1, via a GPCR signaling pathway activated by ChemR23 in nociceptive neurons. RvE1 might represent a new therapeutic target for the treatment of inflammatory pain as a prospective endogenous inhibitor that strongly inhibits TRPV1 activity associated with peripheral inflammation.

scholarly journals Interferon-β suppresses inflammatory pain through activating µ-opioid receptor

2021 ◽  
Vol 17 ◽  
pp. 174480692110452
Author(s):  
Chien Cheng Liu ◽  
I Cheng Lu ◽  
Li Kai Wang ◽  
Jen Yin Chen ◽  
Yu Yu Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Western Blot ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Inflammatory Pain ◽  
Analgesic Effect ◽  
Intrathecal Injection ◽  
Type I ◽  
Withdrawal Threshold ◽  
Withdrawal Latency

Interferons (IFNs) are cytokines secreted by infected cells that can interfere with viral replication. Besides activating antiviral defenses, type I IFNs also exhibit diverse biological functions. IFN-β has been shown to have a protective effect against neurotoxic and inflammatory insults on neurons. Therefore, we aimed to investigate the possible role of IFN-β in reducing mechanical allodynia caused by Complete Freund’s Adjuvant (CFA) injection in rats. We assessed the antinociceptive effect of intrathecal IFN-β in naïve rats and the rats with CFA–induced inflammatory pain. After the behavioral test, the spinal cords of the rats were harvested for western blot and immunohistochemical double staining. We found that intrathecal administration of IFN-β in naïve rats can significantly increase the paw withdrawal threshold and paw withdrawal latency. Further, the intrathecal injection of a neutralizing IFN-β antibody can reduce the paw withdrawal threshold and paw withdrawal latency, suggesting that IFN-β is produced in the spinal cord in normal conditions and serves as a tonic inhibitor of pain. In addition, intrathecal injection of IFN-β at dosages from 1000 U to 10000 U demonstrates a significant transient dose-dependent inhibition of CFA-induced inflammatory pain. This analgesic effect is reversed by intrathecal naloxone, suggesting that IFN-β produces an analgesic effect through central opioid receptor-mediated signaling. Increased expression of phospho-µ-opioid receptors after IFN-β injection was observed on western blot, and immunohistochemical staining showed that µ-opioids co-localized with IFN-α/βR in the dorsal horn of the spinal cord. The findings of this study demonstrate that the analgesic effect of IFN-β is through µ-opioid receptors activation in spial cord.

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