Visceral, inflammatory and neuropathic pain in glycine receptor alpha 3-deficient mice
Visceral, inflammatory and neuropathic pain in glycine receptor alpha 3-deficient mice
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DOI：
10.1097/00001756-200512190-00011
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发表时间：
2005-12-19
期刊：
影响因子：
1.7
通讯作者：
Zimmer, A
中科院分区：
文献类型：
--
作者：
Rácz, D;Schütz, B;Zimmer, A
士的宁敏感甘氨酸受体的α 3亚单位是脊髓前列腺素前列腺素E-2的疼痛增敏作用的重要调节剂。士的宁敏感性甘氨酸受体α 3亚基缺陷的小鼠缺乏前列腺素E-2诱导的甘氨酸能神经传递抑制，并且从炎症诱导的痛觉过敏中恢复得更快。然而，士的宁敏感性甘氨酸受体的α 3亚基是否在涉及前列腺素合成的其他疼痛模型中起作用，如化学诱导的疼痛或神经性疼痛，仍不清楚。在本文中，我们表明，减少醋酸引起的扭体反应的士的宁敏感的甘氨酸受体的α 3-亚基的情况下，但没有变化，在福尔马林引起的疼痛。此外，士的宁敏感的甘氨酸受体缺陷小鼠的α 3-亚基发展正常的热痛觉过敏和触觉异常性疼痛。因此，士的宁敏感性甘氨酸受体的α 3亚基参与调节中度炎症性乙酸诱导的疼痛反应，但既不参与正式的诱导疼痛，也不参与神经性疼痛。NeuroReport 16：2025-2028（c）2005 Lippincott威廉姆斯和威尔金斯。
The alpha 3-subunit of strychnine-sensitive glycine receptors is an important modulator of the pain-sensitizing effects of spinal prostaglandin prostaglandin E-2. Mice deficient for alpha 3-subunit of strychnine-sensitive glycine receptors lack the prostaglandin E-2-induced inhibition of glycinergic neurotransmission and recover faster from inflammation-induced hyperalgesia. It, however, remains unclear whether alpha 3-subunit of strychnine-sensitive glycine receptors plays a role in other pain models involving prostaglandin synthesis, such as chemically induced pain or neuropathic pain. In this paper, we show a reduction of acetic acid-induced writhing responses in the absence of of alpha 3-subunit of strychnine-sensitive glycine receptors, but no changes in formalin-induced pain. Furthermore, alpha 3-subunit of strychnine-sensitive glycine receptors-deficient mice develop normal thermal hyperalgesia and tactile allodynia. Thus, alpha 3-subunit of strychnine-sensitive glycine receptors is involved in the modulation of moderate inflammatory acetic acid-induced pain responses, but neither in formal in-induced pain nor in neuropathic pain. NeuroReport 16:2025-2028 (c) 2005 Lippincott Williams & Wilkins.