TrkA and PKC-epsilon in Thermal Burn–Induced Mechanical Hyperalgesia in the Rat

Summer, Gretchen J.; Puntillo, Kathleen; Miaskowski, Christine; Dina, Olayinka A.; Green, Paul G.; Levine, Jon D.

doi:10.1016/j.jpain.2006.04.009

Cited by 49 publications

(34 citation statements)

References 55 publications

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“…Although human models have been introduced, 124,125,149 it is difficult to separate the mechanisms of burn injury pain in humans. More recently, however, several animal models have been introduced 132,190,200,214 that make it possible to begin to tease apart the complex mechanisms that contribute to the variability and intensity of burn injury pain over time.…”

Section: Basic Science Models Of Burn Injury Painmentioning

confidence: 99%

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Burn Injury Pain: The Continuing Challenge

Summer

Puntillo

Miaskowski

et al. 2007

The Journal of Pain

254

179

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Section: Basic Science Models Of Burn Injury Painmentioning

confidence: 99%

“…In experimental animal models, second-messenger proteins, including protein kinase C-epsilon (PKC⑀) 190 and neurotrophins such as nerve growth factor (NGF) 190,195 have been identified as significant mediators of acute burn-induced hyperalgesia. These mediators may also play a role in chronic burn pain.…”

Section: Basic Science Models Of Burn Injury Painmentioning

confidence: 99%

Burn Injury Pain: The Continuing Challenge

Summer

Puntillo

Miaskowski

et al. 2007

The Journal of Pain

254

179

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“…The 19-mer antisense-and mismatch ODN for gp130 were purchased from Invitrogen (San Francisco, CA). The dose of ODN, 80 μg, was based on prior dose-response curve studies (Summer et al, 2006).…”

Section: Antisense Oligodeoxynucleotide (Odn) Preparationmentioning

confidence: 99%

Role of interleukin-6 in chronic muscle hyperalgesic priming

2008

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After recovery from acute muscle pain even minor subsequent muscle use can initiate recurrence of the same mechanical hyperalgesia months or years after the initial injury. We have recently developed a model of this chronic latent hyperalgesia in the rat. In this study, we have examined the possibility that IL-6, an inflammatory mediator produced during acute muscle inflammation, can mediate the production of this chronic latent hyperalgesic state in which subsequent exposure to inflammatory mediators produce a markedly prolonged mechanical hyperalgesia. We now report that intramuscular injection of IL-6 produced mechanical hyperalgesia, lasting several hours, that was prevented by intrathecal injection of antisense to gp130, an IL-6 receptor subunit. Furthermore, following complete recovery from intramuscular IL-6-induced hyperalgesia, intramuscular PGE 2 produced a mechanical hyperalgesia that was remarkably prolonged compared to naïve controls, indicating the presence of chronic latent hyperalgesia. This ability of IL-6 to produce chronic latent hyperalgesia was prevented by intrathecal admininstration of antisense for gp130. Furthermore, gp130 antisense also prevented chronic latent hyperalgesia produced by intramuscular injection of the inflammogen, carrageenan. These results identify a role for IL-6 in acute inflammatory muscle pain and as a potential target against which therapies might be directed to treat chronic muscle pain.

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“…It has been suggested that burn injury may trigger an immune or inflammatory response that contributes to hyperalgesia, which can persist after burns are healed [11][12][13][14]. Activation of p38 mitogen-activated protein kinase within spinal microglia has been demonstrated in a first-degree burn injury model, and evidence suggests that these glial cells can contribute to the pathogenesis of pain [15].…”

Section: Introductionmentioning

confidence: 99%

Extraterritorial temperature pain threshold abnormalities in subjects with healed thermal injury

Fischer¹,

Waxman²

2012

JRRD

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Abstract-Approximately 1.25 million individuals sustain burn injuries annually in the United States. Pain is frequent in patients with burn injuries and is often refractory to pharmacotherapy. We report quantitative sensory data from five subjects who sustained external thermal injuries to their limb(s) 8 weeks to 11 years previously, demonstrating reduced thermal pain thresholds in regions outside the burn injury zone, including contralateral limbs. Warm and cold detection thresholds were not significantly different from controls. These results complement data from animal models that demonstrate that allodynia can develop contralateral to a focal burn injury as a result of changes within the spinal cord and suggest that systemic or central mechanisms contribute to pain after burn injury.

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TrkA and PKC-epsilon in Thermal Burn–Induced Mechanical Hyperalgesia in the Rat

Cited by 49 publications

References 55 publications

Burn Injury Pain: The Continuing Challenge

Burn Injury Pain: The Continuing Challenge

Role of interleukin-6 in chronic muscle hyperalgesic priming

Extraterritorial temperature pain threshold abnormalities in subjects with healed thermal injury

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