Articles: hyperalgesia.
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Anesthesia and analgesia · Oct 2014
Glycogen Synthase Kinase-3β Inhibition Prevents Remifentanil-Induced Postoperative Hyperalgesia via Regulating the Expression and Function of AMPA Receptors.
Many studies have confirmed that brief remifentanil exposure can enhance pain sensitivity. We previously reported that activation of glycogen synthase kinase-3β (GSK-3β) contributes to remifentanil-induced hyperalgesia via regulating N-methyl-D-aspartate receptor plasticity in the spinal dorsal horn. In this study, we demonstrated that GSK-3β inhibition prevented remifentanil-induced postoperative hyperalgesia via regulating α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) expression and function in the spinal dorsal horn. ⋯ These results indicate that amelioration of remifentanil-induced postoperative hyperalgesia by GSK-3β inhibition is attributed to downregulated AMPAR GluR1 expression in the membrane fraction and inhibition of AMPAR function via altering pGluR1 and Rab5 expression in the spinal dorsal horn.
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This study aims to investigate the presence of bilateral pressure pain hypersensitivity in arm trunk nerves and upper limb mechanosensitivity in breast cancer patients with neck-shoulder pain after medical treatments. ⋯ Breast cancer survivors present bilateral and widespread neural hypersensitivity, as they did in muscular tissue in previous studies. Breast cancer survivors demonstrate a reduction in ROM during ULNTs in the affected side.
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Pannexin 1 (panx1) is a large-pore membrane channel expressed in many tissues of mammals, including neurons and glial cells. Panx1 channels are highly permeable to calcium and adenosine triphosphatase (ATP); on the other hand, they can be opened by ATP and glutamate, two crucial molecules for acute and chronic pain signaling in the spinal cord dorsal horn, thus suggesting that panx1 could be a key component for the generation of central sensitization during persistent pain. In this study, we examined the effect of three panx1 blockers, namely, 10panx peptide, carbenoxolone, and probenecid, on C-reflex wind-up activity and mechanical nociceptive behavior in a spared nerve injury neuropathic rat model involving sural nerve transection. ⋯ Intrathecal administration of the panx1 blockers significantly depressed the spinal C-reflex wind-up activity in both neuropathic and sham control rats, and decreased mechanical hyperalgesia in neuropathic rats without affecting the nociceptive threshold in sham animals. Western blotting showed that panx1 was similarly expressed in the dorsal horn of lumbar spinal cord from neuropathic and sham rats. The present results constitute the first evidence that panx1 channels play a significant role in the mechanisms underlying central sensitization in neuropathic pain.
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One of the major unresolved issues in treating pain is the paradoxical hyperalgesia produced by opiates, and accumulating evidence implicate that EphBs receptors and ephrinBs ligands are involved in mediation of spinal nociceptive information and central sensitization, but the manner in which ephrinB/EphB signalling acts on spinal nociceptive information networks to produce hyperalgesia remains enigmatic. The objective of this research was to investigate the role of ephrinB/EphB signalling in remifentanil-induced hyperalgesia (RIH) and its downstream effector. ⋯ Our findings indicated that ephrinB/EphB signalling is involved in RIH. EphrinB/EphB signalling might be the upstream of NMDA receptor.
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Quantitative sensory testing (QST) has been used to elucidate the peripheral and central mechanisms that underlie changes in pain sensitivity associated with low back pain (LBP). However, it remains unclear to what degree peripheral and central changes contribute to the generation and maintenance of LBP. The aim of this study was to compare thermal pain sensitivity, measured using QST, in participants with acute LBP, chronic LBP, and pain-free controls. ⋯ We found evidence for localized and generalized cold hyperalgesia in chronic, but not acute LBP. We might speculate that hyperalgesia develops as a consequence of long-lasting LBP, but prospective studies are needed to confirm this assumption.