Ferreira S H, Lorenzetti B B
Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, USP, Brazil.
Inflamm Res. 1996 Oct;45(10):499-502. doi: 10.1007/BF02311085.
The present investigation was aimed at assessing the involvement of primary sensory neurons in the hyperalgesia induced by the intrathecal injection of PGE2, as well as whether the hyperalgesic effect was due to the spinal release of glutamate.
Male Wistar rats were used.
Hyperalgesia was measured using the rat paw pressure test.
Intrathecal PGE2 (2.5-50 ng/rat) administration caused a dose-dependent hyperalgesia in both paws. Ipsilateral intraplantar injections of morphine (0.5-8 micrograms/paw) or SNAP (S-nitroso-N-acetyl-D,L-penicillamine, 50-200) micrograms/paw) dose-dependently antagonized spinally-induced PGE2 hyperalgesia (ANOVA, p < 0.001). Their antinociceptive effects were confirmed to be peripheral by abolition following pretreatment of the paws with L-NMMA (NG-monomethyl-L-arginine monoacetate), 50 micrograms/paw or with methylene blue (500 micrograms/paw). The spinally-induced PGE2 hyperalgesia was antagonized by intrathecal injections (9 micrograms) of AP5 (2-amino-5-phosphonopentanoate/2-amino-5) a selective NMDA receptor antagonist.
Intrathecal administration of PGE2 seems to cause hyperalgesia by spinal sensitization of the primary afferent neuron through the release of glutamate.
本研究旨在评估初级感觉神经元在鞘内注射前列腺素E2（PGE2）诱导的痛觉过敏中的作用，以及痛觉过敏效应是否归因于脊髓中谷氨酸的释放。
使用雄性Wistar大鼠。
采用大鼠 paw 压力测试来测量痛觉过敏。
鞘内注射PGE2（2.5 - 50 ng/只大鼠）在两只爪子上均引起剂量依赖性痛觉过敏。同侧足底注射吗啡（0.5 - 8微克/只爪子）或SNAP（S-亚硝基-N-乙酰-D,L-青霉胺，50 - 200微克/只爪子）剂量依赖性地拮抗脊髓诱导的PGE2痛觉过敏（方差分析，p < 0.001）。在用L-NMMA（NG-单甲基-L-精氨酸单乙酸盐）50微克/只爪子或亚甲蓝（500微克/只爪子）预处理爪子后，其镇痛作用通过消除得以证实是外周性的。鞘内注射（9微克）AP5（2-氨基-5-膦酰戊酸/2-氨基-5）一种选择性NMDA受体拮抗剂可拮抗脊髓诱导的PGE2痛觉过敏。
鞘内注射PGE2似乎通过谷氨酸的释放使初级传入神经元发生脊髓敏化从而导致痛觉过敏。
