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首页> 外文期刊>Experimental Animals >Hallucinogenic 5-Hydroxytryptamine 2A Recepto Agonist Effects in Senescence-Accelerated Mice
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Hallucinogenic 5-Hydroxytryptamine 2A Recepto Agonist Effects in Senescence-Accelerated Mice

机译：致幻性5-羟色胺2A受体激动剂在衰老加速小鼠中的作用

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摘要

Many neuropharmacological agents modulate the activity and conformation of heptahelical G protein-coupled receptors and activate ligand-specific signaling pathways. The hallucinogenic chemical 1-[2,5-dimethoxy-4-iodophenyl]-2-aminopropane (DOI), a serotonin receptor 2A (5-HT2AR) agonist, evokes extracellular signal-regulated kinase 1/2 (ERK1/2) signaling and head-twitch behavior. We previously reported that the senescence accelerated-prone mouse 6 (SAMP6) exhibited altered emotional behavior and increased levels of a serotonin-biosynthesizing enzyme compared to the senescence accelerated-resistant mouse 1 (SAMR1); however, the mechanism underlying the relationship between specific receptor signaling and behavioral phenotypes was unclear. In this study, we performed head-twitch tests and examined the total and phosphorylated levels of ERK1/2 and cAMP-responsive element-binding protein (CREB) in the bilateral somatosensory cortex to assess the differences between SAMP6 and SAMR1 using DOI. Although DOI dose-dependently increased the head-twitch response in both strains, the responses of SAMP6 given 0.3 and 1.0 mg/kg DOI were significantly greater than those of SAMR1 given DOI at the same doses. Although no dose-dependent increase in total ERK1/2 and total CREB expression was detected in response to DOI, the levels of phospho-ERK1/2 and -CREB increased in both strains. The phospho-ERK1/2 and -CREB levels in SAMP6 given 0.3 and 1.0 mg/kg DOI were significantly higher than those in SAMR1 given DOI at the same doses. These results indicate that SAMP6 increases DOI-dependent ERK1/2-CREB signaling leading to more head-twitch responses than SAMR1, and that SAMP6 could provide a useful model for examining the relationship between 5-HT2AR regulatory signaling and behavioral phenotypes.
机译：许多神经药物可以调节七螺旋G蛋白偶联受体的活性和构象，并激活配体特异性信号通路。致幻化学物质1- [2,5-二甲氧基-4-碘苯基] -2-氨基丙烷（DOI）是血清素受体2A（5-HT2AR）激动剂，可引起细胞外信号调节激酶1/2（ERK1 / 2）信号传导和头部抽搐的行为。我们先前曾报道，与抗衰老加速的小鼠1（SAMR1）相比，易衰老加速的小鼠6（SAMP6）表现出改变的情绪行为和5-羟色胺生物合成酶水平的增加；然而，具体受体信号转导和行为表型之间的关系的机制尚不清楚。在这项研究中，我们进行了头部抽搐测试，并检查了双侧体感皮层中ERK1 / 2和cAMP反应元件结合蛋白（CREB）的总磷酸化水平，并使用DOI评估了SAMP6和SAMR1之间的差异。尽管DOI剂量依赖性地增加了两种菌株的头部抽搐反应，但在相同剂量下，给予0.3和1.0 mg / kg DOI的SAMP6的反应显着大于给予SAM的SAMR1的反应。尽管未响应DOI检测到总ERK1 / 2和总CREB表达的剂量依赖性增加，但两种菌株中磷酸-ERK1 / 2和-CREB的水平均增加。给予0.3和1.0 mg / kg DOI的SAMP6中的磷酸化ERK1 / 2和-CREB水平显着高于相同剂量给予DOI的SAMR1中的磷酸化。这些结果表明，SAMP6比SAMR1增加依赖DOI的ERK1 / 2-CREB信号传导，导致更多的头部抽搐反应，并且SAMP6可以为检查5-HT2AR调节信号传导与行为表型之间的关系提供有用的模型。

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  • 来源
    《Experimental Animals》 |2010年第4期|P.441-447|共7页
  • 作者

    Kimie NIIMI; Eiki TAKAHASHI; Chitoshi ITAKURA;

  • 作者单位

    Brain Science and Life Technology Research Foundation, 1-28-12 Narimasu, Itabashi, Tokyo 175-0094, Japan Research Resources Center, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan;

    Research Resources Center, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan;

    Research Resources Center, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    DOI; SAM; signaling pathway;

    机译：DOI;SAM;信号通路;

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