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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1994-10-20
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pubmed:abstractText |
In order to investigate the involvement of glutamate receptor systems in allodynia induced by prostaglandin (PG) E2 or F2 alpha, we co-administered antagonists for N-methyl-D-aspartate (NMDA), non-NMDA, or metabotropic glutamate receptors intrathecally with PGE2 or PGF2 alpha and examined their effects on the allodynia evoked in conscious mice by non-noxious brushing of the flanks. MK-801, a non-competitive NMDA receptor channel blocker, and D-AP-5, a selective NMDA receptor antagonist, dose-dependently blocked PGE2-induced allodynia with an IC50 of 1.60 and 0.52 microgram/mouse, respectively. A glycine binding-site antagonist for the NMDA receptor, 7-Cl-KYNA, did not influence it. None of these NMDA receptor antagonists inhibited PGF2 alpha-evoked allodynia. Non-NMDA receptor antagonists GAMS and CNQX inhibited both PGE2- and PGF2 alpha-induced allodynia. On the other hand, L-AP-3 and L-AP-4, putative metabotropic glutamate receptor antagonists, dose-dependently antagonized the allodynia induced by PGF2 alpha with an IC50 of 0.92 and 3.26 ng/mouse, respectively, but not that induced by PGE2. Intrathecal administration of L-glutamate produced allodynia over a wide range of low doses from 0.1 pg to 0.1 microgram/mouse, and the maximal effect was observed at 1 ng. Similar to allodynia induced by prostaglandins, the response lasted over a 50-min experimental period. These results demonstrate that both PGE2- and PGF2 alpha-evoked allodynia are mediated through a pathway that includes the glutamate receptor system but that subtypes of glutamate receptors involved and sites of action in the spinal cord may be different between them.
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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/Dinoprost,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamates,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0304-3959
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
57
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
225-31
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7916453-Animals,
pubmed-meshheading:7916453-Dinoprost,
pubmed-meshheading:7916453-Dinoprostone,
pubmed-meshheading:7916453-Glutamates,
pubmed-meshheading:7916453-Glutamic Acid,
pubmed-meshheading:7916453-Injections, Spinal,
pubmed-meshheading:7916453-Mice,
pubmed-meshheading:7916453-Neurotransmitter Agents,
pubmed-meshheading:7916453-Pain,
pubmed-meshheading:7916453-Receptors, Metabotropic Glutamate,
pubmed-meshheading:7916453-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:7916453-Spinal Cord,
pubmed-meshheading:7916453-Synaptic Transmission
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pubmed:year |
1994
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pubmed:articleTitle |
Involvement of glutamate receptors in allodynia induced by prostaglandins E2 and F2 alpha injected into conscious mice.
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pubmed:affiliation |
Department of Anesthesiology, Osaka Medical College, Takatsuki, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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