Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2001-7-4
pubmed:abstractText
Neurons in the rostroventromedial medulla (RVM) project to spinal loci where the neurons inhibit or facilitate pain transmission. Abnormal activity of facilitatory processes may thus represent a mechanism of chronic pain. This possibility and the phenotype of RVM cells that might underlie experimental neuropathic pain were investigated. Cells expressing mu-opioid receptors were targeted with a single microinjection of saporin conjugated to the mu-opioid agonist dermorphin; unconjugated saporin and dermorphin were used as controls. RVM dermorphin-saporin, but not dermorphin or saporin, significantly decreased cells expressing mu-opioid receptor transcript. RVM dermorphin, saporin, or dermorphin-saporin did not change baseline hindpaw sensitivity to non-noxious or noxious stimuli. Spinal nerve ligation (SNL) injury in rats pretreated with RVM dermorphin-saporin failed to elicit the expected increase in sensitivity to non-noxious mechanical or noxious thermal stimuli applied to the paw. RVM dermorphin or saporin did not alter SNL-induced experimental pain, and no pretreatment affected the responses of sham-operated groups. This protective effect of dermorphin-saporin against SNL-induced pain was blocked by beta-funaltrexamine, a selective mu-opioid receptor antagonist, indicating specific interaction of dermorphin-saporin with the mu-opioid receptor. RVM microinjection of dermorphin-saporin, but not of dermorphin or saporin, in animals previously undergoing SNL showed a time-related reversal of the SNL-induced experimental pain to preinjury baseline levels. Thus, loss of RVM mu receptor-expressing cells both prevents and reverses experimental neuropathic pain. The data support the hypothesis that inappropriate tonic-descending facilitation may underlie some chronic pain states and offer new possibilities for the design of therapeutic strategies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Immunotoxins, http://linkedlifedata.com/resource/pubmed/chemical/N-Glycosyl Hydrolases, http://linkedlifedata.com/resource/pubmed/chemical/Naltrexone, http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides, http://linkedlifedata.com/resource/pubmed/chemical/Opioid Peptides, http://linkedlifedata.com/resource/pubmed/chemical/Plant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Ribosome Inactivating Proteins..., http://linkedlifedata.com/resource/pubmed/chemical/beta-funaltrexamine, http://linkedlifedata.com/resource/pubmed/chemical/dermorphin, http://linkedlifedata.com/resource/pubmed/chemical/saporin
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5281-8
pubmed:dateRevised
2008-7-12
pubmed:meshHeading
pubmed-meshheading:11438603-Animals, pubmed-meshheading:11438603-Behavior, Animal, pubmed-meshheading:11438603-Brain Stem, pubmed-meshheading:11438603-Disease Models, Animal, pubmed-meshheading:11438603-Immunotoxins, pubmed-meshheading:11438603-Ligation, pubmed-meshheading:11438603-Male, pubmed-meshheading:11438603-Medulla Oblongata, pubmed-meshheading:11438603-Microinjections, pubmed-meshheading:11438603-N-Glycosyl Hydrolases, pubmed-meshheading:11438603-Naltrexone, pubmed-meshheading:11438603-Neuralgia, pubmed-meshheading:11438603-Neurons, pubmed-meshheading:11438603-Oligopeptides, pubmed-meshheading:11438603-Opioid Peptides, pubmed-meshheading:11438603-Pain Measurement, pubmed-meshheading:11438603-Physical Stimulation, pubmed-meshheading:11438603-Plant Proteins, pubmed-meshheading:11438603-Radioligand Assay, pubmed-meshheading:11438603-Rats, pubmed-meshheading:11438603-Rats, Sprague-Dawley, pubmed-meshheading:11438603-Reaction Time, pubmed-meshheading:11438603-Receptors, Opioid, mu, pubmed-meshheading:11438603-Recombinant Fusion Proteins, pubmed-meshheading:11438603-Ribosome Inactivating Proteins, Type 1, pubmed-meshheading:11438603-Spinal Nerves
pubmed:year
2001
pubmed:articleTitle
Inhibition of neuropathic pain by selective ablation of brainstem medullary cells expressing the mu-opioid receptor.
pubmed:affiliation
Departments of Pharmacology and Anesthesiology, University of Arizona, Tucson, Arizona 85724, USA. frankp@u.arizona.edu
pubmed:publicationType
Journal Article