Inhibition of hyperalgesia by ablation of lamina I spinal neurons expressing the substance P receptor
Inhibition of hyperalgesia by ablation of lamina I spinal neurons expressing the substance P receptor
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DOI：
10.1126/science.278.5336.275
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发表时间：
1997-10-10
期刊：
影响因子：
56.9
通讯作者：
Simone, DA
中科院分区：
文献类型：
--
作者：
Mantyh, PW;Rogers, SD;Simone, DA
P物质在疼痛刺激时在脊髓中释放，但其在伤害性信号传导中的作用尚不清楚。当P物质和核糖体失活蛋白皂草素的缀合物被注入脊髓时，它被内化并对表达P物质受体的脊髓I层神经元具有细胞毒性。这种治疗使对轻度伤害性刺激的反应保持不变，但明显减弱了对高度伤害性刺激的反应以及机械和热痛觉过敏。因此，表达P物质受体的脊髓I层神经元在高度伤害性刺激的传递和痛觉过敏的维持中起关键作用。
Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear, When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.