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Altered nociception, analgesia and aggression in mice lacking the receptor for substance P (see comments)

机译：缺乏P物质受体的小鼠的伤害感受，镇痛作用和攻击性发生了变化（请参阅评论）

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摘要

The peptide neurotransmitter substance P modulates sensitivity to pain by activating the neurokinin-1 (NK-1) receptor, which is expressed by discrete populations of neurons throughout the central nervous system. Substance P is synthesized by small-diameter sensory 'pain' fibres, and release of the peptide into the dorsal horn of the spinal cord following intense peripheral stimulation promotes central hyperexcitability and increased sensitivity to pain. However, despite the availability of specific NK-1 antagonists, the function of substance P in the perception of pain remains unclear. Here we investigate the effect of disrupting the gene encoding the NK-1 receptor in mice. We found that the mutant mice were healthy and fertile, but the characteristic amplification ('wind up') and intensity coding of nociceptive reflexes was absent. Although substance P did not mediate the signalling of acute pain or hyperalgesia, it was essential for the full development of stress-induced analgesia and for an aggressive response to territorial challenge, demonstrating that the peptide plays an unexpected role in the adaptive response to stress.
机译：肽神经递质P通过激活神经激肽-1（NK-1）受体来调节对疼痛的敏感性，该受体由整个中枢神经系统中离散的神经元群体表达。 P物质是由小直径的感觉“疼痛”纤维合成的，在强烈的外周刺激后，肽释放到脊髓的背角中促进了中央过度兴奋性和对疼痛的敏感性增加。然而，尽管可获得特定的NK-1拮抗剂，但P物质在感知疼痛中的功能仍不清楚。在这里，我们研究了破坏小鼠中编码NK-1受体的基因的作用。我们发现，突变小鼠既健康又可育，但是缺乏伤害性反射的特征性扩增（“结束”）和强度编码。尽管P物质不介导急性疼痛或痛觉过敏的信号传导，但它对于充分发展应激诱导的镇痛作用以及对领土挑战的积极反应至关重要，表明该肽在对应激的适应性反应中发挥了意想不到的作用。

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