TY - JOUR
T1 - Intracerebroventricular injection of prostaglandin E2 induces thermal hyperalgesia in rats
T2 - the possible involvement of EP3 receptors
AU - Oka, Takakazu
AU - Aou, Shuji
AU - Hori, Tetsuro
N1 - Funding Information:
The followingc ompoundws ere gifts which the authors gratefullya cknowledgeS: C19220from Dr. G. Fleet, Searle,U SA; butaprosftr om Dr. P.J. Gardiner, Bayer, UK; M&B28767 from Dr. L. Webb, Rhone-Poulenc,U K. We also expresso ur gratitudeto Drs. Y. Watanabe(O sakaB iochemicaIln stitute)S, . Narumiya (Kyoto UniversityS choolof Medicine) and K. Mizu-mura (Instituteo f EnvironmentaMl edicine,Nagoya Universityf)o r providingin formationa boutEP receptors agonistsa nd antagonistsW. e are gratefult o B.C. Quinn, Kyushu Universityf,o r readingt he manuscript. This work was performedth roughS pecialCoordina-tion Funds of the Sciencea nd TechnologyA gencyof the JapaneseG overnmen(tt o T. Hori) and was also supportedin part by Grant-in-Aid for ScientificR e-searcho n Priority Areas 'Pain' (03260102to T. Hori) and Grant-in-Aid for Scientific Research( 06454153 and 06557006to T. Hori) from the Ministry of Education, Sciencea, nd Culture,J apan.
PY - 1994/11/14
Y1 - 1994/11/14
N2 - To determine what types of prostanoid receptors are involved in the central effect of prostaglandin E2 (PGE2) on nociception, we administered PGE2 and its agonists, i.e., 17-phenyl-ω-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonists), 11-deoxy PGE1 (an EP2/EP3 receptor agonist, EP2 ≫ EP3) and M&B28767 (an EP3 receptor agonist) into the lateral cerebroventricle (LCV) of rats and observed the changes of paw-withdrawal latency on a hot plate. The LCV injection of PGE2 (10 pg/kg-10 ng/kg), 11-deoxy PGE1 (100 pg/kg-10 ng/kg) and M&B28767 (1 pg/kg-100 pg/kg) produced a significant reduction in the paw-withdrawal latency. The maximal reduction was observed 15 min after the LCV injection of these drugs. Neither 17-phenyl-ω-trinor PGE2 (1 pg/kg-1 μg/kg) nor butaprost (1 pg/kg-100 μg/kg) induced any significant changes in the paw-withdrawal latency. The LCV injection of PGE2 (1 μg/kg) and 17-phenyl-ω-trinor PGE2 (50 μg/kg) increased the latency only 5 min after LCV injection. These findings indicate that the LCV injection of PGE2 induces thermal hyperalgesia through EP3 receptors and analgesia through EP1 receptors by its central action in rats.
AB - To determine what types of prostanoid receptors are involved in the central effect of prostaglandin E2 (PGE2) on nociception, we administered PGE2 and its agonists, i.e., 17-phenyl-ω-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonists), 11-deoxy PGE1 (an EP2/EP3 receptor agonist, EP2 ≫ EP3) and M&B28767 (an EP3 receptor agonist) into the lateral cerebroventricle (LCV) of rats and observed the changes of paw-withdrawal latency on a hot plate. The LCV injection of PGE2 (10 pg/kg-10 ng/kg), 11-deoxy PGE1 (100 pg/kg-10 ng/kg) and M&B28767 (1 pg/kg-100 pg/kg) produced a significant reduction in the paw-withdrawal latency. The maximal reduction was observed 15 min after the LCV injection of these drugs. Neither 17-phenyl-ω-trinor PGE2 (1 pg/kg-1 μg/kg) nor butaprost (1 pg/kg-100 μg/kg) induced any significant changes in the paw-withdrawal latency. The LCV injection of PGE2 (1 μg/kg) and 17-phenyl-ω-trinor PGE2 (50 μg/kg) increased the latency only 5 min after LCV injection. These findings indicate that the LCV injection of PGE2 induces thermal hyperalgesia through EP3 receptors and analgesia through EP1 receptors by its central action in rats.
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U2 - 10.1016/0006-8993(94)91275-0
DO - 10.1016/0006-8993(94)91275-0
M3 - Article
C2 - 7874513
AN - SCOPUS:0028143593
SN - 0006-8993
VL - 663
SP - 287
EP - 292
JO - Brain Research
JF - Brain Research
IS - 2
ER -