Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-2-14
pubmed:abstractText
Spinal cord injury (SCI) commonly results in the development of neuropathic pain, which can dramatically impair the quality of life for SCI patients. SCI-induced neuropathic pain can be manifested as both tactile allodynia (a painful sensation to a non-noxious stimulus) and hyperalgesia (an enhanced sensation to a painful stimulus). The mechanisms underlying these pain states are poorly understood. Clinical studies have shown that gabapentin, a drug that binds to the voltage-gated calcium channel alpha-2-delta-1 subunit (Ca(v)?2?-1) proteins is effective in the management of SCI-induced neuropathic pain. Accordingly, we hypothesized that tactile allodynia post SCI is mediated by an upregulation of Ca(v)?2?-1 in dorsal spinal cord. To test this hypothesis, we examined whether SCI-induced dysregulation of spinal Ca(v)?2?-1 plays a contributory role in below-level allodynia development in a rat spinal T9 contusion injury model. We found that Ca(v)?2?-1 expression levels were significantly increased in L4-6 dorsal, but not ventral, spinal cord of SCI rats that correlated with tactile allodynia development in the hind paw plantar surface. Furthermore, both intrathecal gabapentin treatment and blocking SCI-induced Ca(v)?2?-1 protein upregulation by intrathecal Ca(v)?2?-1 antisense oligodeoxynucleotides could reverse tactile allodynia in SCI rats. These findings support that SCI-induced Ca(v)?2?-1 upregulation in spinal dorsal horn is a key component in mediating below-level neuropathic pain states, and selectively targeting this pathway may provide effective pain relief for SCI patients. Spinal cord contusion injury caused increased calcium channel Ca(v)?2?-1 subunit expression in dorsal spinal cord that contributes to neuropathic pain states.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1872-6623
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
649-55
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:21239111-Amines, pubmed-meshheading:21239111-Analgesics, pubmed-meshheading:21239111-Animals, pubmed-meshheading:21239111-Calcium Channels, pubmed-meshheading:21239111-Cyclohexanecarboxylic Acids, pubmed-meshheading:21239111-Disease Models, Animal, pubmed-meshheading:21239111-Dose-Response Relationship, Drug, pubmed-meshheading:21239111-Double-Blind Method, pubmed-meshheading:21239111-Female, pubmed-meshheading:21239111-Hyperalgesia, pubmed-meshheading:21239111-Motor Activity, pubmed-meshheading:21239111-Neuralgia, pubmed-meshheading:21239111-Oligodeoxyribonucleotides, Antisense, pubmed-meshheading:21239111-Pain Measurement, pubmed-meshheading:21239111-Pain Threshold, pubmed-meshheading:21239111-Rats, pubmed-meshheading:21239111-Rats, Sprague-Dawley, pubmed-meshheading:21239111-Recovery of Function, pubmed-meshheading:21239111-Spinal Cord, pubmed-meshheading:21239111-Spinal Cord Injuries, pubmed-meshheading:21239111-Statistics as Topic, pubmed-meshheading:21239111-Time Factors, pubmed-meshheading:21239111-Up-Regulation, pubmed-meshheading:21239111-gamma-Aminobutyric Acid
pubmed:year
2011
pubmed:articleTitle
Calcium channel alpha-2-delta-1 protein upregulation in dorsal spinal cord mediates spinal cord injury-induced neuropathic pain states.
pubmed:affiliation
Department of Pharmacology, University of California Irvine, School of Medicine, Irvine, CA 92697, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural