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脑钠肽(BNP)表达感觉神经元不参与急性、炎症性或神经性疼痛。

Brain natriuretic peptide (BNP) expressing sensory neurons are not involved in acute, inflammatory or neuropathic pain.

机构信息

Department of Molecular Biomedical Sciences, College of Veterinary Medicine (CVM), NC State University.

出版信息

Mol Pain. 2017 Jan-Dec;13:1744806917736993. doi: 10.1177/1744806917736993.

Abstract

BACKGROUND

We recently demonstrated that brain natriuretic peptide is expressed in the dorsal root ganglia, and that brain natriuretic peptide is required for normal detection of pruritogens. We further showed that the receptor for brain natriuretic peptide, natriuretic peptide receptor A, is present in the spinal cord, and elimination of these neurons profoundly attenuates scratching to itch-inducing compounds. However, the potential modulatory roles of brain natriuretic peptide in nociception, inflammation, and neuropathic mechanisms underlying the sensation of pain have not been investigated in detail.

FINDINGS

To demonstrate the involvement of brain natriuretic peptide in pain, we compared the behavioral responses of brain natriuretic peptide knockout mice with their wild-type littermates. First, we showed that brain natriuretic peptide is not required in chemically induced pain responses evoked by the administration of capsaicin, allyl isothiocyanate, adenosine 5′-triphosphate, or inflammatory soup. We further measured pain behaviors and found no involvement of brain natriuretic peptide in hot, cold, or mechanical nociceptive responses in mice, nor did we find evidence for the involvement of brain natriuretic peptide in neuroinflammatory sensitization elicited by complete Freund’s adjuvant or in neuropathic pain.

CONCLUSIONS

These results demonstrate that brain natriuretic peptide is not essential for pain-related behaviors.

摘要

背景

我们最近证明脑钠肽存在于背根神经节中,并且脑钠肽对于正常检测瘙痒原是必需的。我们进一步表明,脑钠肽的受体,即利钠肽受体 A,存在于脊髓中,消除这些神经元会显著减弱对致痒化合物的搔抓反应。然而,脑钠肽在痛觉感受中的伤害感受、炎症和神经病理性机制中的潜在调节作用尚未被详细研究。

结果

为了证明脑钠肽在疼痛中的参与,我们比较了脑钠肽敲除小鼠与其野生型同窝仔鼠的行为反应。首先,我们表明脑钠肽在由辣椒素、丙烯基异硫氰酸酯、三磷酸腺苷或炎症汤引起的化学诱导性疼痛反应中不是必需的。我们进一步测量了疼痛行为,发现脑钠肽在小鼠的热、冷或机械性伤害感受反应中没有参与,也没有证据表明脑钠肽参与完全弗氏佐剂引起的神经炎症致敏或神经病理性疼痛。

结论

这些结果表明脑钠肽对于与疼痛相关的行为不是必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8604/5639968/19918858004b/10.1177_1744806917736993-fig1.jpg

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