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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Formalin-induced long-term secondary allodynia and hyperalgesia are maintained by descending facilitation.
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Formalin-induced long-term secondary allodynia and hyperalgesia are maintained by descending facilitation.

机译：福尔马林引起的长期继发性异常性疼痛和痛觉过敏通过降低促进作用得以维持。

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This work analyzes the role of cholecystokinin (CCK) receptors, dynorphin A and descending facilitation originated in the rostral ventromedial medulla (RVM) on secondary allodynia and hyperalgesia in formalin-injected rats. Formalin injection (50 muL, 1%, s.c.) produced acute nociception (lasting 1 h) and long-term secondary allodynia and hyperalgesia in ipsilateral and contralateral hind paws (lasting 1-12 days). Once established, intra-RVM administration of lidocaine at day 6, but not at 2, reversed secondary allodynia and hyperalgesia in rats. The injection of YM022 (CCK receptor antagonist), but not lorglumide (CCK receptor antagonist), into the RVM or spinal cord reversed both nociceptive behaviors. Pre-treatment with lidocaine, lorglumide or YM022 did not prevent the development of secondary allodynia or hyperalgesia regardless of the administration route. Formalin injection increased dynorphin content in the dorsal, but not the ventral, spinal cord sections at day 6. Moreover, intrathecal administration of dynorphin antiserum reversed, but was unable to prevent, secondary allodynia and hyperalgesia in both hind paws. These results suggest that formalin-induced secondary allodynia and hyperalgesia are maintained by activation of descending facilitatory mechanisms which are dependent on CCK receptors located in the RVM and spinal cord. In addition, data suggest that spinal dynorphin A and CCK play an important role in formalin-induced secondary allodynia and hyperalgesia.
机译：这项工作分析了在注射福尔马林的大鼠继发性异常性疼痛和痛觉过敏中胆囊收缩素（CCK）受体，强啡肽A和源于延髓腹侧延髓（RVM）的降序促进作用。福尔马林注射液（50μL，1％，s.c.）产生急性伤害（持续1 h），并在同侧和对侧后爪产生长期继发性异常性疼痛和痛觉过敏（持续1-12天）。建立后，在第6天而非第2天进行RVM内利多卡因给药可逆转大鼠继发性异常性疼痛和痛觉过敏。向RVM或脊髓中注射YM022（CCK受体拮抗剂）而不是洛格鲁米德（CCK受体拮抗剂）可逆转这两种伤害行为。利多卡因，洛格鲁米德或YM022的预处理并未阻止继发性异常性疼痛或痛觉过敏的发生，无论其给药途径如何。在第6天，福尔马林注射增加了背部的强啡肽含量，但没有增加腹侧，脊髓区域的强啡肽含量。此外，鞘内注射强啡肽抗血清的作用逆转，但不能预防两只后爪继发性异常性疼痛和痛觉过敏。这些结果表明福尔马林诱导的继发性异常性疼痛和痛觉过敏通过激活依赖于RVM和脊髓中CCK受体的递减促进机制得以维持。此外，数据表明，脊髓强啡肽A和CCK在福尔马林引起的继发性异常性疼痛和痛觉过敏中起重要作用。

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