最近一項發(fā)表在美國國家科學院院刊（Proceedings of the National Academy of Sciences）上的研究闡明了痛覺神經(jīng)遞質(zhì)P物質(zhì)（SP）在痛覺感受及傳導中的作用，為痛覺的研究及治療提供了新的思路,。
SP是一種痛覺神經(jīng)遞質(zhì),，在很多器官中傳導痛覺。雖然肌肉組織和腦脊液中的SP水平過高通常與慢性肌肉痛有關,，但SP在肌肉痛覺的感受和傳遞過程中的作用仍不明確,。
研究者使用缺乏SP信號的小鼠來研究SP在肌肉痛覺敏感性中的作用。他們發(fā)現(xiàn)同SP信號正常的小鼠相比,，缺乏SP信號的小鼠在接受了肌肉內(nèi)注射酸性物質(zhì)之后,，對痛覺的敏感性增高,，這與神經(jīng)遞質(zhì)通常所起的興奮性作用恰好相反。
導致該小鼠肌肉痛覺敏感性增高的原因,，是其缺少SP信號基因并產(chǎn)生一些物質(zhì)與SP受體結合,。這一發(fā)現(xiàn)表明SP或許在肌肉痛覺傳遞中作為抑制劑通過抑制肌肉痛覺受體發(fā)揮作用，并作為抑制反饋通路的一部分在慢性肌肉痛患者身上起作用,。
目前有一些通過減少纖維肌痛患者SP神經(jīng)受體發(fā)揮作用的藥物在進行臨床試驗,，作者告誡這些研究人員須當心這類藥物增加患者慢性肌肉痛以及肌肉痛覺敏感性的風險。（生物谷bioon.com）
doi:10.1073/pnas.1108903108
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An antinociceptive role for substance P in acid-induced chronic muscle pain
An antinociceptive role for substance P in acid-induced chronic muscle pain.
Release of substance P (SP) from nociceptive nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transmission of pain signals. Nonetheless, the role of SP in muscle pain remains unknown. Here we show that a single i.m. acid injection in mice lacking SP signaling by deletion of the tachykinin precursor 1 (Tac1) gene or coadministration of NK1 receptor antagonists produces long-lasting hyperalgesia rather than the transient hyperalgesia seen in control animals. The inhibitory effect of SP was found exclusively in neurons expressing acid-sensing ion channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G protein-independent but tyrosine kinase-dependent manner. Furthermore, the SP signaling could alter action potential thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors. Thus, i.m. SP mediates an unconventional NK1 receptor signal pathway to inhibit acid activation in muscle nociceptors, resulting in an unexpected antinociceptive effect against chronic mechanical hyperalgesia, here induced by repeated i.m. acid injection.
