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脑室内注射前列腺素E2可诱导大鼠热痛觉过敏:EP3受体可能参与其中。

Intracerebroventricular injection of prostaglandin E2 induces thermal hyperalgesia in rats: the possible involvement of EP3 receptors.

作者信息

Oka T, Aou S, Hori T

机构信息

Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Brain Res. 1994 Nov 14;663(2):287-92. doi: 10.1016/0006-8993(94)91275-0.

DOI:10.1016/0006-8993(94)91275-0
PMID:7874513
Abstract

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-omega-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonist), 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-omega-trinor PGE2 (1 pg/kg-1 microgram/kg) nor butaprost (1 pg/kg-100 microgram/kg) induced any significant changes in the paw-withdrawal latency. The LCV injection of PGE2 (1 microgram/kg) and 17-phenyl-omega-trinor PGE2 (50 micrograms/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.

摘要

为了确定何种类型的前列腺素受体参与前列腺素E2(PGE2)对伤害感受的中枢效应,我们将PGE2及其激动剂,即17-苯基-ω-三降PGE2(一种EP1受体激动剂)、布他前列素(一种EP2受体激动剂)、11-脱氧PGE1(一种EP2/EP3受体激动剂,EP2作用远强于EP3)和M&B28767(一种EP3受体激动剂)注入大鼠侧脑室(LCV),并在热板上观察缩爪潜伏期的变化。向侧脑室注射PGE2(10 pg/kg - 10 ng/kg)、11-脱氧PGE1(100 pg/kg - 10 ng/kg)和M&B28767(1 pg/kg - 100 pg/kg)可使缩爪潜伏期显著缩短。在侧脑室注射这些药物15分钟后观察到最大程度的缩短。17-苯基-ω-三降PGE2(1 pg/kg - 1微克/千克)和布他前列素(1 pg/kg - 100微克/千克)均未引起缩爪潜伏期的任何显著变化。侧脑室注射PGE2(1微克/千克)和17-苯基-ω-三降PGE2(50微克/千克)仅在注射后5分钟使潜伏期延长。这些结果表明,侧脑室注射PGE2通过其在大鼠体内的中枢作用,经EP3受体诱导热痛觉过敏,经EP1受体诱导镇痛。

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