Source:http://linkedlifedata.com/resource/pubmed/id/11438603
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
14
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pubmed:dateCreated |
2001-7-4
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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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
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1529-2401
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5281-8
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pubmed:dateRevised |
2008-7-12
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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
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pubmed:year |
2001
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pubmed:articleTitle |
Inhibition of neuropathic pain by selective ablation of brainstem medullary cells expressing the mu-opioid receptor.
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pubmed:affiliation |
Departments of Pharmacology and Anesthesiology, University of Arizona, Tucson, Arizona 85724, USA. frankp@u.arizona.edu
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pubmed:publicationType |
Journal Article
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