Linked Life Data

18419759

Source:http://linkedlifedata.com/resource/pubmed/id/18419759

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-8-8
pubmed:abstractText
A better understanding of the mechanisms linked to chemokine pronociceptive effects is essential for the development of new strategies to better prevent and treat chronic pain. Among chemokines, MCP-1/CCL2 involvement in neuropathic pain processing is now established. However, the mechanisms by which MCP-1/CCL2 exerts its pronociceptive effects are still poorly understood. In the present study, we demonstrate that MCP-1/CCL2 can alter pain neurotransmission in healthy rats. Using immunohistochemical studies, we first show that CCL2 is constitutively expressed by primary afferent neurons and their processes in the dorsal horn of the spinal cord. We also observe that CCL2 is co-localized with pain-related peptides (SP and CGRP) and capsaicin receptor (VR1). Accordingly, using in vitro superfusion system of lumbar dorsal root ganglion and spinal cord explants of healthy rats, we show that potassium or capsaicin evoke calcium-dependent release of CCL2. In vivo, we demonstrate that intrathecal administration of CCL2 to healthy rats produces both thermal hyperalgesia and sustained mechanical allodynia (up to four consecutive days). These pronociceptive effects of CCL2 are completely prevented by the selective CCR2 antagonist (INCB3344), indicating that CCL2-induced pain facilitation is elicited via direct spinal activation of CCR2 receptor. Therefore, preventing the activation of CCR2 might provide a fruitful strategy for treating pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
106
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
757-69
pubmed:meshHeading
pubmed-meshheading:18419759-Analysis of Variance, pubmed-meshheading:18419759-Animals, pubmed-meshheading:18419759-Behavior, Animal, pubmed-meshheading:18419759-Calcitonin Gene-Related Peptide, pubmed-meshheading:18419759-Calcium, pubmed-meshheading:18419759-Chemokine CCL2, pubmed-meshheading:18419759-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:18419759-Ganglia, Spinal, pubmed-meshheading:18419759-Gene Expression Regulation, pubmed-meshheading:18419759-Hyperalgesia, pubmed-meshheading:18419759-Male, pubmed-meshheading:18419759-Neurons, Afferent, pubmed-meshheading:18419759-Pain Threshold, pubmed-meshheading:18419759-Potassium Chloride, pubmed-meshheading:18419759-Pyrrolidines, pubmed-meshheading:18419759-Rats, pubmed-meshheading:18419759-Rats, Sprague-Dawley, pubmed-meshheading:18419759-Receptors, CCR2, pubmed-meshheading:18419759-Spinal Cord, pubmed-meshheading:18419759-Subcellular Fractions, pubmed-meshheading:18419759-Substance P, pubmed-meshheading:18419759-TRPV Cation Channels
pubmed:year
2008
pubmed:articleTitle
Spinal CCL2 pronociceptive action is no longer effective in CCR2 receptor antagonist-treated rats.
pubmed:affiliation
Department of Physiology and Biophysics, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't