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Stimulation of nitric oxide release from rat spinal cord by prostaglandin E 2
Author(s) -
Sakai Masato,
Minami Toshiaki,
Hara Naoki,
Nishihara Isao,
Kitade Hiroaki,
Kamiyama Yasuo,
Okuda Kazuyuki,
Takahashi Hakuo,
Mori Hidemaro,
Ito Seiji
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701661
Subject(s) - prostaglandin e2 receptor , prostaglandin e2 , nmda receptor , chemistry , agonist , receptor antagonist , prostaglandin e , prostaglandin , glutamate receptor , nitric oxide , spinal cord , allodynia , stimulation , endocrinology , medicine , pharmacology , nociception , antagonist , receptor , hyperalgesia , biology , neuroscience , biochemistry
1 We recently demonstrated that intrathecal administration of prostaglandin E 2 (PGE 2 ) and PGF 2α induced allodynia through a pathway that includes the glutamate receptor and nitric oxide (NO)‐generating systems from pharmacological studies. In order to clarify the involvement of NO in prostaglandin‐induced allodynia, we measured NO released from rat spinal cord slices by a chemiluminescence method. 2 PGE 2 stimulated NO release from both dorsal and ventral regions all along the spinal cord. PGE 2 stimulated the release within 10 min and increased it in a time‐dependent manner. 3 The PGE 2 ‐induced NO release was observed at 100 n M –10 μ M . PGF 2α stimulated the release at concentrations higher than 1 μ M , but PGD 2 (up to 10 μ M ) did not enhance it. 4 17‐Phenyl‐ω‐trinor PGE 2 (EP 1 >EP 3 ) and sulprostone (EP 1