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Inflammatory pain severely affects the quality of life of millions of individuals worldwide. Prostaglandin E2 (PGE2), a pain mediator enriched in inflamed tissues, plays a pivotal role in nociceptor sensitization and in the genesis of inflammatory pain. Its EP4 receptor mainly mediates its role in inflammatory pain. However, the underlying mechanisms are poorly understood. Here we found that PGE2/EP4...
Tolerance to morphine-induced analgesia is an intractable phenomenon, often hindering its prolonged applications in the clinics. The enhanced pronociceptive actions of spinal pain-related molecules such as calcitonin gene-related peptide (CGRP) may underlie this phenomenon and could be a promising target for intervention. We demonstrate here how CGRP regulates the development of morphine analgesic...
Studies implicate endocannabinoids in the acute and chronic actions of opioid drugs, including the genesis of physical dependence. Previous evidence suggests that spinal release of calcitonin gene-related peptide (CGRP) and activation of its receptors contribute to opioid physical dependence. The release of CGRP at the spinal level is modulated by cannabinoid (CB 1 )-receptors. Thus, this...
Some electrophysiologic studies demonstrate new, excitatory α2-adrenoceptors on peripheral nociceptors and their dorsal root ganglion (DRG) cell bodies after nerve injury, yet administration of α2-adrenoceptor agonists at these sites reduces hypersensitivity rather than worsens it. Since TRPV-1 expressing nociceptor afferents are important in many pain states, we examined the expression of this channel...
The activation of glial cells in the spinal dorsal horn and the gracile nucleus by inflammation and nerve injury has been suggested to be involved in neuronal plasticity and central sensitization, hence contributing to tactile allodynia. The aim of this study was to determine the possible intracellular signal transduction pathway associated with glial cells, which have been activated by partial sciatic...
Activation of adenosine A1 receptors by endogenous adenosine or synthetic agonists produces anti-nociception in animal models of acute pain and also reduces hypersensitivity in models of inflammatory and nerve-injury pain. Allosteric adenosine modulators facilitate adenosine agonist binding to the A1 receptor. The purpose of the current study was to examine the effect, mechanisms of action, and interaction...
Partial sciatic nerve injury causes neuropathic pain associated with behavioral changes such as spontaneous pain, hyperalgesia and allodynia. Both central and peripheral sensitization of pain pathways are likely to be involved in these alterations. Nerve injury induced plastic changes in the dorsal horn, where the second relay nociceptive neurons are located, may contribute to the central sensitization...
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