• Remifentanil was delivered intravenously in rats to induce hyperalgesia. (iasp-pain.org)
  • Our data revealed that spinal DMT1(-)IRE and iron content significantly increased in remifentanil-treated rats, and MK-801 inhibited the enhancements. (iasp-pain.org)
  • Specifically, this study determined immunoreactivity of a peptidergic pro-nociceptive transmitter (substance P) and one of its receptors, neurokinin-1 (NK-1) receptor, in spinal cord dorsal horns in rats performing a HRNF reaching task for 6-10 weeks. (cdc.gov)
  • The relationship of these spinal cord changes with the number of TNFa immunopositive cells in flexor forelimb muscles and with previously observed forearm grip strength changes from these same rats were examined. (cdc.gov)
  • We hypothesized that CRF-CRFR1 signaling in central amygdala (CeA) mediates stress-induced hyperalgesia in rats with high stress reactivity. (nature.com)
  • Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyperalgesic effect of systemic CRFR1 antagonist in stressed rats. (nature.com)
  • These data suggest that rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in CeA. (nature.com)
  • In the first of such studies, the remote antinociceptive effects of simulated spinal mobilization were determined in adult rats with inflammatory hindpaw nociception [ 19 ]. (hindawi.com)
  • Three minutes of spinal mobilization was delivered to 6 restrained rats at approximately 2 Hertz (Hz) with the experimenter's finger over the lumbar (L5) spinous process beginning 10 minutes after intraplantar hindpaw injection of a mixture of endogenous inflammatory mediators. (hindawi.com)
  • Intraperitoneal (i.p.) injection of kainic acid induced a persistent thermal hyperalgesia, when tested using the hot plate (mice) and tail flick (mice and rats) assays, and mechanical hyperalgesia when tested using von Frey monofilaments (rats), but had no effect on acetic acid-induced chemical nociception (mice). (biopsychiatry.com)
  • Recent studies have shown that UVB irradiation induces primary and secondary hyperalgesia in rats and humans peaking about 24 h after UVB exposure. (lu.se)
  • Furthermore, although the VR1-null mice appeared normal in a wide range of behavioural tests, including responses to acute noxious thermal stimuli, their ability to develop carrageenan-induced thermal hyperalgesia was completely absent. (nih.gov)
  • Systemic blockade of corticotropin-releasing factor (CRF) type 1 receptors (CRFR1s) reduces stress-induced thermal hyperalgesia. (nature.com)
  • Avoiders exhibited thermal hyperalgesia that was reversed by systemic or intra-CeA injection of a CRFR1 antagonist. (nature.com)
  • We have previously described the changes in spinal cord neuropeptides in the unilateral sciatic chronic constriction injury (CCI) model of Bennett and Xie [Pain, 33 (1988) 87-108] at 28 days, a time of maximum mechanical hyperalgesia. (ox.ac.uk)
  • Mechanical hyperalgesia was assessed with a Ugo-Basile analgesymeter and immunohistochemistry performed on the spinal cord sections of the animals and quantified using a confocal microscope. (ox.ac.uk)
  • Pressure pain thresholds of the inflamed hindpaws were increased (decreased mechanical sensitivity) immediately after spinal mobilization ended. (hindawi.com)
  • Semmes-Weinstein monofilaments (Stoelting Company, Wood Dale, IL) was used to test for mechanical hyperalgesia. (koreamed.org)
  • Because TRPV4 appears to be more important in pathological pain conditions than in normal mechanical nociception, we investigated whether TRPV4 also is involved in mechanical hyperalgesia associated with painful peripheral neuropathy. (jneurosci.org)
  • Cyclooxygenase-2 (COX-2)-dependent prostaglandin (PG) E2 synthesis in the spinal cord plays a major role in the development of inflammatory hyperalgesia and allodynia. (uni-frankfurt.de)
  • It has been described that individuals with TMD could display diffuse hyperalgesia and allodynia 3 3. (scielo.br)
  • It has been described that individuals with TMD could display diffuse hyperalgesia and allodynia 3-4 and it was suggested that they have a fundamental problem with pain or sensory processing rather than an abnormality confined to a specific region of the body where pain is perceived to originate 5-6 . (bvsalud.org)
  • 2009). Microinjection of angiotensin II in the caudal ventrolateral medulla induces hyperalgesia . (up.pt)
  • When injected intrathecally (i.t.), kainic acid itself failed to induce hyperalgesia and AMPA/KA antagonists given i.t. also failed to attenuate the hyperalgesic effect of kainic acid administered i.p., indicating that the spinal cord is not the primary site of action. (biopsychiatry.com)
  • This study presents that aberrant iron accumulation is involved in the development of remifentanil-induced hyperalgesia in vivo and in vitro. (iasp-pain.org)
  • We report that the lipoxin A, receptor is expressed on spinal astrocytes both in vivo and in vitro and that spinal delivery of lipoxin A, as well as stable analogues, attenuates inflammation-induced pain. (harvard.edu)
  • Histological evaluation of rat spinal cord and dorsal root ganglia revealed no neurodegenerative changes 24 h after kainic acid. (biopsychiatry.com)
  • Spinal cord stimulation is a non-neurodestructive and reversible technique that is extremely helpful in treating refractory neuropathic pain. (massgeneral.org)
  • indicates that morphine-induced hyperalgesia, as neuropathic pain, is a pathological alteration of pain sensitivity whose expression is gated by spinal microglia. (atsbio.com)
  • We found that curcumin administered intrathecally or orally significantly attenuated hyperalgesia in mice with morphine-induced OIH. (uic.edu)
  • Surprisingly, intrathecally administered FTY720 reduced the nociceptive behaviour in the formalin assay without altering spinal prostaglandin synthesis, indicating that additional antinociceptive mechanisms beside the inhibition of prostaglandin synthesis are involved. (uni-frankfurt.de)
  • A ) A representative cervical spinal dorsal horn section obtained from a rat which was subcutaneously injected with morphine for 10 days (10 mg/kg) and intrathecally injected with Mac-1-SAP (20 mcg) during the last 3 days. (atsbio.com)
  • Furthermore, we demonstrated that the effects of curcumin on OIH correlated with the suppression of chronic morphine-induced CaMKIIα activation in the superficial laminae of the spinal dorsal horn. (uic.edu)
  • While this peripheral inflammatory pain model allowed for a demonstration of an immediate remote antinociceptive effect following spinal mobilization, investigating the effect's duration requires a model with longer-lasting nociception. (hindawi.com)
  • To build upon the findings from the study of spinal mobilization's antinociceptive effects on inflamed hindpaw nociception [ 19 ], we chose to use the formalin test to produce hindpaw inflammatory pain remote to the anatomical treatment site. (hindawi.com)
  • To our knowledge, no other laboratories are examining spinal cord nociceptive neurochemicals in response to repetitive motion-induced injury and inflammation. (cdc.gov)
  • Thus, our highly repetitive task leads to increased spinal cord pro-nociceptive neurochemicals that are most likely directed by forelimb muscle inflammation and pain. (cdc.gov)
  • Targeting mechanisms that counterregulate the spinal consequences of persistent peripheral inflammation provide a novel endogenous mechanism by which chronic pain may be controlled. (harvard.edu)
  • Performance of the HRNF task resulted in significantly increased substance P and NK-1 receptor immunoreactivity in the superficial lamina of spinal cord dorsal horns at 6 and 10 weeks compared to trained controls (p (cdc.gov)
  • This increased pain sensation might be related with lowered vesicular zinc level in the superficial gray matter in the spinal cord. (koreamed.org)
  • NMDA receptor modulates spinal iron accumulation via activating DMT1(-)IRE in remifentanil-induced hyperalgesia. (iasp-pain.org)
  • N-methyl-D-aspartate (NMDA) receptor activation is known to be critical in remifentanil-induced hyperalgesia. (iasp-pain.org)
  • This study suggests that DMT1(-)IRE-mediated iron accumulation is likely to be the downstream event following NMDA receptor activation and Ca influx, contributing to remifentanil-induced hyperalgesia. (iasp-pain.org)
  • Together these data suggest that a persistent hyperalgesia results from the transient activation of AMPA/KA receptors that are located outside the spinal cord, perhaps on the distal projections of primary afferent fibers. (biopsychiatry.com)
  • The increased substance P and NK-1 receptor immmunoreactivity were positively correlated with declines in forearm grip strength, an assay of movement-related hyperalgesia (r = 0.70, p (cdc.gov)
  • However, examination of the lumbar spinal cord revealed the following changes. (ox.ac.uk)
  • We ligated a left-sided lumbar spinal nerve with silk under anesthesia using pentobarbital (50 mg/kg). (koreamed.org)
  • The density of zinc was significantly decreased in zinc concentration in the dorsal horn of 4th, 5th and 6th lumbar segments at 5 and 10 days after the spinal nerve ligation. (koreamed.org)
  • Figure at right: Microglia depletion in the lumbar region of the spinal cord after intrathecal injections of Mac-1-SAP (Cat. (atsbio.com)
  • B ) A representative lumbar spinal dorsal horn section from the same rat showing the decrease in OX-42 staining after Mac-1-SAP treatment. (atsbio.com)
  • Optimizing pain relief resulting from spinal manipulative therapies, including low velocity variable amplitude spinal manipulation (LVVA-SM), requires determining their mechanisms. (hindawi.com)
  • Importantly, spinal cords and primary spinal cord cells derived from mPGES-1-deficient mice showed a redirection of the PGE2 synthesis to PGD2, PGF2α and 6-keto-PGF1α (stable metabolite of PGI2). (uni-frankfurt.de)
  • This study was designed to investigate any correlation between the mechanism of pain development and changes of histochemically-reactive zinc contents in the rat spinal cords following peripheal nerve ligation. (koreamed.org)
  • It actually changes nerve function along patients' spinal cords, said Michael Robinson, director of the UF Center for Pain Research and Behavioral Health. (medicalxpress.com)
  • Traumatic spinal cord injury (SCI) is perhaps the most devastating orthopedic injury, and with prolonged survival being the rule, rehabilitation of these injuries has an increasingly important role. (medscape.com)
  • The Spinal Cord Injury Rehabilitation (SCIRehab) project , a 5-year project led by the Rocky Mountain Regional Spinal Injury System (RMRSIS) at Craig Hospital, used practice-based evidence (PBE) research to identify the rehabilitation interventions most strongly associated with positive outcomes. (medscape.com)
  • Surprisingly, in the COX-2-dependent zymosan-evoked hyperalgesia model, the nociceptive behavior was not reduced in mPGES-1-deficient mice despite a marked decrease of the spinal PGE2 synthesis. (uni-frankfurt.de)
  • In this study we examine the same model 100-120 days post injury by which time resolution of the hyperalgesia and peripheral nerve injury has occurred according to previous studies. (ox.ac.uk)
  • These results indicate that changes in neuronal markers in the spinal cord can persist after apparent resolution of a peripheral nerve injury. (ox.ac.uk)
  • Hyperalgesia is an exaggerated response to noxious stimuli produced by peripheral or central plasticity. (nature.com)
  • Hyperalgesia is an exaggerated and prolonged response to noxious stimuli that can be produced by plasticity at peripheral sites (eg, reduced threshold and/or amplified nociceptor response to noxious stimuli) and centrally in the spinal cord or brain. (nature.com)
  • This hyperalgesia reflects sensitization of peripheral terminals and facilitation of pain signaling at the spinal level. (harvard.edu)
  • The anti inflammatory role of peripheral lipoxins raises the hypothesis that similar neuraxial systems may also down-regulate injury-induced spinal facilitation of pain processing. (harvard.edu)
  • An increase in the expression of the prodynorphin (proDYN) gene was noted after reinflammation in the spinal cord ipsilateral to the afferents of the neonatally treated hind paw. (tmu.edu.tw)
  • iii) NPY levels in laminae 3 and 4 of the spinal cord showed a 15% increase in immunoreactivity compared to sham animals (P = 0.008). (ox.ac.uk)
  • In the present study we investigated the changes in galanin, substance P and c-fos immunoreactivity in rat DRG and spinal cord at the L5 level 2-96 h after UVB irradiation. (lu.se)
  • In the spinal cord, UVB irradiation induced increased immunoreactivity for galanin in the dorsal horn, the area around the central canal and interestingly also in the lateral spinal nucleus 12-96 h after exposure. (lu.se)
  • At the CTPR, I am currently the principal investigator for five IRB-approved research projects focused on understanding the science behind how spinal cord stimulation therapy reduces pain. (massgeneral.org)
  • He said hyperalgesia is a phenomenon in which the nervous system becomes sensitized to stimulation, amplifying the intensity perceived by the patient. (medicalxpress.com)
  • When administered i.p., 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an (R,S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid HBr/kainate (AMPA/KA) antagonist, completely blocked hyperalgesia. (biopsychiatry.com)
  • In this study, we examined the effects of performing a voluntary, highly repetitive , negligible force (HRNF) reaching task on spinal cord neurochemicals involved in nociception. (cdc.gov)
  • In the affected ventral spinal cord, resveratrol enhanced the expression of several vascular endothelial growth factor family proteins (VEGFs) and increased the phosphorylation of p300 through Akt signaling, indicating activation of p300 acetyltransferase. (vinomis.com)
  • Resveratrol activated p300 acetyltransferase-mediated VEGF signaling in the affected ventral spinal cord, which may have thus contributed to the acceleration of nerve regeneration and motor repair. (vinomis.com)
  • Kainic acid injected subcutaneously in the back of mice decreased response latencies in the hot plate and tail flick assays, indicating that hyperalgesia is achieved by a variety of parenteral routes of injection. (biopsychiatry.com)
  • Furthermore, activation of extracellular signal-regulated kinase and c-Jun N-terminal kinase in astrocytes, which has been indicated to play an important role in spinal pain processing, was attenuated in the presence of lipoxins. (harvard.edu)
  • This linkage opens the possibility that lipoxins regulate spinal nociceptive processing though their actions upon astrocytic activation. (harvard.edu)
  • CeA projections to periacqueductal gray (PAG) gate descending pathways that modulate nociceptive afferent activity in the dorsal horn of the spinal cord. (nature.com)
  • Injury-induced hyperalgesia. (webmd.com)
  • Growing evidence suggests that proinflammatory cytokines (PICs), such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNFα), are induced in the spinal cord under various injury conditions and contribute to pain hypersensitivity. (jneurosci.org)
  • Results from both spinal manipulation and spinal mobilization studies in asymptomatic and symptomatic individuals demonstrate short-term pain relief both remote and local to the anatomical treatment site following a single treatment [ 5 - 16 ]. (hindawi.com)
  • We also demonstrate that Taxol-induced TRPV4-mediated hyperalgesia is essentially dependent on integrin/Src tyrosine kinase signaling. (jneurosci.org)