Primary afferent tachykinins are required to experience moderate to intense pain
Primary afferent tachykinins are required to experience moderate to intense pain
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DOI：
10.1038/32897
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发表时间：
1998-03-26
期刊：
影响因子：
64.8
通讯作者：
Basbaum, AI
中科院分区：
文献类型：
--
作者：
Cao, YQ;Mantyh, PW;Basbaum, AI
兴奋性神经递质谷氨酸盐与被称为P物质的肽共存于对疼痛刺激做出反应的初级传入神经中（1）。由于谷氨酸受体阻断剂确实能减少疼痛行为（2-4），因此假定“疼痛”信息是由背角神经元上的谷氨酸作用介导的。然而，P物质的作用仍不清楚。我们现在已经破坏了小鼠前速激肽A基因（PPT-A），该基因编码P物质和相关的速激肽，神经激肽A（参考文献5）。我们发现，虽然这些小鼠对轻度疼痛刺激的行为反应是完整的，但对中度至剧烈疼痛的反应显着减少。由外周释放P物质和神经激肽A（参考文献6）引起的神经源性炎症在突变小鼠中几乎不存在。我们的结论是，释放速激肽从初级传入痛觉感受器（伤害性感受器）是需要产生中度至强烈的疼痛。
The excitatory neurotransmitter glutamate coexists,vith the peptide known as substance P in primary afferents that respond to painful stimulation(1). Because blockers of glutamate receptors reliably reduce pain behaviour(2-4), it is assumed that 'pain' messages are mediated by glutamate action on dorsal horn neurons, The contribution of substance P, however, is still unclear, We have now disrupted the mouse preprotachykinin A gene (PPT-A), which encodes substance P and a related tachykinin, neurokinin A (ref. 5). We find that although the behavioural response to mildly painful stimuli is intact in these mice, the response to moderate to intense pain is significantly reduced. Neurogenic inflammation, which results from peripheral release of substance P and neurokinin A (ref. 6), is almost absent in the mutant mice. We conclude that the release of tachykinins from primary afferent pain-sensing receptors (nociceptors) is required to produce moderate to intense pain.