Comparison of mice deficient in the high- or low-affinity neurotensin receptors, Ntsr1 or Ntsr2, reveals a novel function for Ntsr2 in thermal nociception
Comparison of mice deficient in the high- or low-affinity neurotensin receptors, Ntsr1 or Ntsr2, reveals a novel function for Ntsr2 in thermal nociception
复制标题
DOI：
10.1016/j.brainres.2003.11.039
复制
发表时间：
2004-02-13
期刊：
影响因子：
2.9
通讯作者：
Wada, KJ
中科院分区：
文献类型：
--
作者：
Maeno, H;Yamada, K;Wada, KJ
神经紧张素（NT）是一种神经肽，可诱导广泛的生物活性，包括低温和镇痛。这些作用是由NT受体Ntsr1、Ntsr2和Ntsr3介导的，尽管每种受体在特定NT功能中的作用尚不清楚。为了研究体内的伤害功能，我们制造了ntsr1缺陷和ntsr2缺陷的小鼠。此外，Ntsr1和Ntsr2 mrna在参与nt相关伤害感觉的小鼠大脑区域进行了组织化学分析。Ntsr2 mRNA在肾导水管周围灰质（PAG）和延髓吻侧腹侧（RVM）的表达量大于Ntsr1。对突变小鼠和对照小鼠进行热痛觉检测，在热板实验中，与ntsr1缺陷小鼠或野生型对照小鼠相比，ntsr2缺陷小鼠的跳跃潜伏期发生了显著变化。与对照组相比，突变小鼠的甩尾和舔后爪潜伏期未受影响。这些结果表明，与Ntsr1相比，Ntsr2在热痛觉中具有重要作用，这些突变小鼠可能为开发镇痛药物提供了有用的工具。(C) 2003 Elsevier B.V.版权所有
Neurotensin (NT) is a neuropeptide that induces a wide range of biological activities including hypothermia and analgesia. Such effects are mediated by the NT receptors Ntsr1, Ntsr2 and Ntsr3, although the involvement of each receptor in specific NT functions remains unknown. To address nociceptive function in vivo, we generated both Ntsr1-deficient and Ntsr2-deficient mice. In addition, histochemical analyses of both Ntsr1 and Ntsr2 mRNAs were performed in the mouse brain regions involved in NT-related nociception. The expression of Ntsr2 mRNA was greater than that of Ntsr1 in the periaqueductal gray (PAG) and the rostral ventral medulla (RVM). The mutant and control mice were subjected to the examination of thermal nociception, and in the hot plate test, a significant alteration in jump latency was observed in Ntsr2-deficient mice compared to Ntsr1-deficient or wild-type control mice. Latencies of tail flick and hind paw licking of the mutant mice were not affected compared to control mice. These results suggest that Ntsr2 has an important role in thermal nociception compared to Ntsr1, and that these mutant mice may represent a useful tool for the development of analgesic drugs. (C) 2003 Elsevier B.V. All rights reserved.