Source:http://linkedlifedata.com/resource/pubmed/id/18477704
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2008-7-10
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pubmed:abstractText |
Glucose-sensitive neurons in the lateral hypothalamic area produce orexin-A (OxA) as well as orexin-B (OxB) and send their axons to the spinal dorsal horn, which predominantly expresses orexin receptor-1 (OX-1), showing a higher sensitivity to OxA. The purpose of the present study was to assess the effects of OxA on the induction of a novel form of activity-dependent reflex potentiation, spinal reflex potentiation (SRP), in the pelvic-urethral reflex activity. External urethra sphincter electromyogram in response to pelvic afferent nerve test stimulation (TS; 1/30 Hz) or repetitive stimulation (RS; 1 Hz) was recorded in anesthetized rats. TS evoked a baseline reflex activity, whereas RS produced SRP, which was abolished by intrathecal OxA (30 nM, 10 mul). Intrathecal SB-408124 (10 muM, 10 mul), an OX-1 antagonist, reversed the abolition on SRP caused by OxA. Although there is, so far, no NR2A- and NR2B-specific agonist available, N-methyl-d-aspartate (NMDA) reversed the abolition on the RS-induced SRP caused by the co-administration of OxA and Co-101244 (30 nM, 10 mul; an NMDA NR2B subunit antagonist), but it did not reverse the abolition by the co-administration of OxA and PPPA (300 nM, 10 mul; an NMDA NR2A subunit antagonist). In conclusion, the activation of descending orexinergic fibers may inhibit the repetitive afferent input-induced central sensitization of pelvic-urethral reflex activity and urethra hyperactivity, indicating that spinal orexinergic neural transmission may be a novel target for the treatment of patients with neuropathetic or postinflammatory pain of pelvic origin.
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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/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/NR2B NMDA receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptides,
http://linkedlifedata.com/resource/pubmed/chemical/PD 174494,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate,
http://linkedlifedata.com/resource/pubmed/chemical/SDZ EAA 494,
http://linkedlifedata.com/resource/pubmed/chemical/orexins
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0193-1849
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
295
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E117-29
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pubmed:meshHeading |
pubmed-meshheading:18477704-Action Potentials,
pubmed-meshheading:18477704-Animals,
pubmed-meshheading:18477704-Electromyography,
pubmed-meshheading:18477704-Excitatory Amino Acid Antagonists,
pubmed-meshheading:18477704-Female,
pubmed-meshheading:18477704-Immunohistochemistry,
pubmed-meshheading:18477704-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:18477704-N-Methylaspartate,
pubmed-meshheading:18477704-Neurons, Afferent,
pubmed-meshheading:18477704-Neuropeptides,
pubmed-meshheading:18477704-Piperazines,
pubmed-meshheading:18477704-Piperidines,
pubmed-meshheading:18477704-Rats,
pubmed-meshheading:18477704-Rats, Wistar,
pubmed-meshheading:18477704-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:18477704-Reflex,
pubmed-meshheading:18477704-Spinal Cord,
pubmed-meshheading:18477704-Synaptic Transmission,
pubmed-meshheading:18477704-Urethra
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pubmed:year |
2008
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pubmed:articleTitle |
Orexin-A modulates glutamatergic NMDA-dependent spinal reflex potentiation via inhibition of NR2B subunit.
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pubmed:affiliation |
Department of Physiology, College of Medicine, Chung-Shan Medical University Hospital, 110, Chang-Kuo North Rd., Section 1, Taichung, Taiwan .
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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