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速激肽1基因靶向缺失小鼠的痛觉减退

Hypoalgesia in mice with a targeted deletion of the tachykinin 1 gene.

作者信息

Zimmer A, Zimmer A M, Baffi J, Usdin T, Reynolds K, König M, Palkovits M, Mezey E

机构信息

Section on Genetics, National Institute of Mental Health, Bethesda, MD 20892, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2630-5. doi: 10.1073/pnas.95.5.2630.

Abstract

The tachykinin neuropeptides, substance P and substance K, are produced in nociceptive primary sensory neurons and in many brain regions involved in pain signaling. However, the precise role and importance of these neuropeptides in pain responses has been debated. We now show that mice that cannot produce these peptides display no significant pain responses following formalin injection and have an increased pain threshold in the hotplate test. On the other hand, the mutant mice react normally in the tail flick assay and acetic acid-induced writhing tests. These results demonstrate that substance P and/or substance K have essential functions in specific responses to pain.

摘要

速激肽神经肽,即P物质和K物质,由伤害性初级感觉神经元以及许多参与疼痛信号传导的脑区产生。然而,这些神经肽在疼痛反应中的确切作用和重要性一直存在争议。我们现在表明,无法产生这些肽的小鼠在福尔马林注射后没有明显的疼痛反应,并且在热板试验中的疼痛阈值有所提高。另一方面,突变小鼠在甩尾试验和醋酸诱导的扭体试验中反应正常。这些结果表明,P物质和/或K物质在对疼痛的特定反应中具有重要功能。

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