TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat.

TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Research Abstract Details 

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TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Abstract Text:

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

Although mechanical hyperalgesia associated with medical procedures is the major source of severe pain in burn-injured patients, little is known about its underlying mechanism. One reason for this has been the lack of a model for mechanical hyperalgesia at the site of injury. We have modified an established partial-thickness burn model in the rat to produce long-lasting primary mechanical hyperalgesia, which is present from the first measurement at 0.5 h, reaches a maximum at 3 days, and is still significant after 7 days. Because nerve growth factor (NGF), which is elevated in burn-injured tissue, produces mechanical hyperalgesia and activates protein kinase C (PKC)-epsilon, a key mediator in inflammatory and neuropathic pain, we used this model to evaluate the role of the NGF receptor, tyrosine-receptor kinase A (TrkA), and PKC-epsilon in burn-induced primary mechanical hyperalgesia. Intrathecal administration of antisense oligodeoxynucleotides to TrkA and PKC-epsilon, starting 3 days before inducing a burn injury, caused dose-related decrease of burn-induced primary mechanical hyperalgesia. In addition, intradermal injection of a PKC-epsilon-selective inhibitor eliminated hyperalgesia. Our model provides a method to elucidate the underlying mechanism of burn-injury pain as well as to screen for targets for novel analgesic treatments of this important clinical condition. PERSPECTIVE: This manuscript presents the first model of thermal injury-induced mechanical hyperalgesia which mimics prolonged duration of clinical burn injury pain. We also perform proof of concept experiments demonstrating that our model provides a method to elucidate the mechanism of this important clinical condition.

TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Publishing Authors By Initials

GJ Summer,KA Puntillo,C Miaskowski,OA Dina,PG Green,JD Levine,

For similar natural sciences: time: time factors research abstracts see: natural sciences: time: time factors research

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TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The journal of pain : official journal of the Amer

VOLUME: 7

Page Numbers: 884-91

Journal Abbreviation:

ISSN: 1526-5900

DAY: 3

MONTH: Dec

YEAR: 2006

TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100898657

TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Keywords Mesh Terms:

KEYWORDS: Time Factors

MESH TERMS: metabolism

Chemical & Substance for Abstract: TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat. Information

Substance Name: Protein Kinase C-epsilon

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for TrkA and PKC-epsilon in thermal burn-induced mechanical hyperalgesia in the rat.

AFFILIATION: Department of Physiological Nursing, School of Nursing, University of California, San Francisco, USA. gretchen.summer@ucsf.edu

Country: United States

AGENCY: United States NIDCR

GRANT: R01-DE08973

ACRONYM: DE

MEDLINETA: J Pain

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