Endogenous μ-opioid - neuropeptide Y Y1 receptor synergy silences chronic postoperative pain
Nelson, T. S.; Santos, D. F. S.; Prasoon, P.; Gralinski, M.; Allen, H. N.; Taylor, B. K.
Show abstract
Tissue injury creates a delicate balance between latent pain sensitization (LS) and compensatory endogenous analgesia. Inhibitory G protein-coupled receptor (GPCR) interactions that oppose LS, including -opioid receptor (MOR) and neuropeptide Y Y1 receptor (Y1R) activity, persist in the spinal cord dorsal horn (DH) for months, even after the resolution of normal pain thresholds. Here, we demonstrate that following recovery from surgical incision, a potent endogenous analgesic synergy between MOR and Y1R activity persists within DH interneurons to reduce the intensity and duration of latent postoperative hyperalgesia and ongoing pain. Failure of such endogenous GPCR signaling to maintain LS in remission may underlie the transition from acute to chronic pain states.
Matching journals
The top 5 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Protective role of neuronal and lymphoid cannabinoid CB2 receptors in neuropathic pain 98%
- Cellular Mechanisms Underlying Central Sensitization in a Mouse Model of Chronic Muscle Pain 97%
- Loss of cortical control over the descending pain modulatory system determines the development of the neuropathic pain state in rats 97%
Similar papers in this journal
- Endogenous inflammatory mediators produced by injury activate TRPV1 and TRPA1 nociceptors to induce sexually dimorphic cold pain that is dependent on TRPM8 and GFRalpha3 97%
- Neuroendocrine mechanisms governing sex-differences in chronic pain involve prolactin receptor sensory neuron signaling 96%
- Type I interferons act directly on nociceptors to produce pain sensitization: Implications for viral infection-induced pain 96%
Similar papers in this journal
- A role for protease activated receptor type 3 (PAR3) in nociception demonstrated through development of a novel peptide agonist 97%
- Mouse models of non-dystrophic and dystrophic myotonia exhibit nociplastic pain-like behaviors 97%
- De novo expression of neuropeptide Y in sensory neurons does not contribute to peripheral neuropathic pain 96%
Similar papers in this journal
- Studies on CRMP2 SUMOylation-deficient transgenic mice identify sex-specific NaV1.7 regulation in the pathogenesis of chronic neuropathic pain 94%
- The role of amygdala calcitonin gene-related peptide receptors on the development of persistent bladder pain in mice. 94%
- Lysophosphatidyl-choline 16:0 mediates persistent joint pain through Acid-Sensing Ion Channel 3: preclinical and clinical evidences 94%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.