Hosoi M, Oka T, Hori T
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Pain. 1997 Jul;71(3):303-11. doi: 10.1016/s0304-3959(97)03380-0.
The effects of microinjection of prostaglandin E2 (PGE2) (0.5 fg-500 pg/0.2 microl) into the medial part of the preoptic area (MPO) on nociception were studied using a hot-plate test in rats. The intraMPO microinjection of PGE2 only at non-pyrogenic doses (5-50 fg) reduced the paw-withdrawal latency, suggesting hyperalgesia. Maximal reduction was obtained 15 min after the injection of PGE2 at 50 fg. Subsequently, to determine which types of prostanoid receptors are involved in the hyperalgesic effect of PGE2 in the MPO, we administered PGE2 receptor agonists, i.e., 17-phenyl-omega-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonist) and M&B28767 (an EP3 receptor agonist) into the MPO and observed the nociceptive behavior. The intraMPO injection of M&B28767 (0.005 fg-50 pg), like that of PGE2, exhibited a U-shaped dose response characteristic, i.e., a significant decrease of the paw-withdrawal latency only at 0.05-5 fg with the maximal response at 0.5 fg. However, neither the administration of EP1 (0.5 fg-50 ng) nor EP2 (0.5 fg-500 pg) agonists had any effect on nociception. The microinjection of M&B28767 at 0.5 fg into the other parts of preoptic hypothalamus (the lateral part of the preoptic area and the median preoptic nucleus) and the diagonal band of Broca (DBB) produced hyperalgesia similar to the intraMPO-induced hyperalgesia in terms of magnitude and time course. Microinjection of M&B28767 (0.5 fg) into either the paraventricular nucleus, the ventromedial hypothalamus, the lateral hypothalamic area or the septal nucleus had no effect on nociception. These findings suggest that PGE2 at non-pyrogenic doses in the brain induces hyperalgesia, at least in part, through its actions on EP3 receptors in the preoptic hypothalamus and the DBB in rats.
采用热板试验,研究了向大鼠视前区内侧(MPO)微量注射前列腺素E2(PGE2)(0.5飞克 - 500皮克/0.2微升)对伤害感受的影响。仅在非致热剂量(5 - 50飞克)下向MPO内微量注射PGE2会缩短爪部撤离潜伏期,提示痛觉过敏。注射50飞克PGE2后15分钟出现最大程度的缩短。随后,为确定哪些类型的前列腺素受体参与了PGE2在MPO中的痛觉过敏作用,我们将PGE2受体激动剂,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)和M&B28767(一种EP3受体激动剂)注入MPO,并观察伤害感受行为。向MPO内注射M&B28767(0.005飞克 - 50皮克),与注射PGE2类似,呈现出U形剂量反应特征,即仅在0.05 - 5飞克时爪部撤离潜伏期显著缩短,在0.5飞克时出现最大反应。然而,注射EP1激动剂(0.5飞克 - 50纳克)和EP2激动剂(0.5飞克 - 500皮克)均对伤害感受无任何影响。向视前下丘脑的其他部位(视前区外侧和视前正中核)以及Broca斜带(DBB)微量注射0.5飞克的M&B28767,在程度和时间进程方面产生了与MPO内注射诱导的痛觉过敏相似的痛觉过敏。向室旁核、腹内侧下丘脑、外侧下丘脑区或隔核微量注射M&B28767(0.5飞克)对伤害感受无影响。这些发现表明,脑中非致热剂量的PGE2至少部分通过其对视前下丘脑和大鼠DBB中EP3受体的作用诱导痛觉过敏。