Deltamethrin (DM), a type II pyrethroid, robustly increases brain-derived neurotrophic factor (Bdnf) expression and has a neurotrophic effect in primary cultures of rat cortical neurons. In this study, we investigated the effect of DM on neurite morphology in cultured rat cortical neurons. DM significantly increased neurite outgrowth, but this increase was abolished when the BDNF scavenger tropomyosin receptor kinase B (TrkB)-Fc was added 10 min before the DM treatment. In contrast, the addition of TrkB-Fc 1 h after the treatment did not affect DM-induced neurite outgrowth. Our previous research has indicated that type II, but not type I, pyrethroids have the ability to induce Bdnf mRNA expression, but neither permethrin nor cypermethrin, which are type I and type II pyrethroids, respectively, affected neurite outgrowth in the current study. These results suggest that this effect is not due to increased Bdnf expression, and the effect is unique to DM. We previously demonstrated that calcineurin plays a role in the DM-mediated induction of Bdnf expression. However, the calcineurin inhibitor FK506 did not significantly affect DM-induced neurite outgrowth. DM-induced neurite outgrowth was abolished by U0126 and rapamycin, indicating the involvement of the mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) pathways. Taken together, these findings suggest that DM activates endogenous BDNF/TrkB-mediated MAPK and mTOR pathways, thereby increasing neurite outgrowth.Key words: BDNF, Deltamethrin, MAPK, mTOR, Neurite outgrowth.

中文翻译：

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溴氰菊酯通过内源性BDNF / TrkB途径增加皮质神经元的神经突生长。

溴氰菊酯（DM）是一种II类拟除虫菊酯，可强烈增加脑源性神经营养因子（Bdnf）的表达，并在大鼠皮质神经元的原代培养物中具有神经营养作用。在这项研究中，我们调查了DM对培养的大鼠皮质神经元神经突形态的影响。DM显着增加了神经突增生，但是当在DM治疗前10分钟添加BDNF清道夫原肌球蛋白受体激酶B（TrkB）-Fc时，这种增加被消除。相反，在处理后1小时加入TrkB-Fc不影响DM诱导的神经突增生。我们以前的研究表明，II型拟除虫菊酯具有诱导Bdnf mRNA表达的能力，但在当前研究中，分别为I型和II型拟除虫菊酯的氯菊酯和氯氰菊酯均不影响神经突的生长。这些结果表明该效应不是由于增加的Bdnf表达，并且该效应是DM特有的。我们以前证明钙调神经磷酸酶在DM介导的Bdnf表达诱导中发挥作用。但是，钙调神经磷酸酶抑制剂FK506不会显着影响DM诱导的神经突增生。DM引起的神经突增生被U0126和雷帕霉素消除，表明有丝分裂原激活的蛋白激酶（MAPK）和哺乳动物雷帕霉素靶标（mTOR）通路的参与。综上所述，这些发现提示DM激活内源性BDNF / TrkB介导的MAPK和mTOR途径，从而增加神经突的生长。关键词：BDNF，溴氰菊酯，MAPK，mTOR，神经突的生长。我们以前证明钙调神经磷酸酶在DM介导的Bdnf表达诱导中起作用。但是，钙调神经磷酸酶抑制剂FK506不会显着影响DM诱导的神经突增生。DM引起的神经突增生被U0126和雷帕霉素消除，表明有丝分裂原激活的蛋白激酶（MAPK）和哺乳动物雷帕霉素靶标（mTOR）通路的参与。综上所述，这些发现表明DM激活内源性BDNF / TrkB介导的MAPK和mTOR途径，从而增加了神经突的生长。关键词：BDNF，溴氰菊酯，MAPK，mTOR，神经突的生长。我们以前证明钙调神经磷酸酶在DM介导的Bdnf表达诱导中发挥作用。但是，钙调神经磷酸酶抑制剂FK506不会显着影响DM诱导的神经突增生。DM引起的神经突增生被U0126和雷帕霉素消除，表明有丝分裂原激活的蛋白激酶（MAPK）和哺乳动物雷帕霉素靶标（mTOR）通路的参与。综上所述，这些发现表明DM激活内源性BDNF / TrkB介导的MAPK和mTOR途径，从而增加了神经突的生长。关键词：BDNF，溴氰菊酯，MAPK，mTOR，神经突的生长。表明有丝分裂原激活的蛋白激酶（MAPK）和哺乳动物雷帕霉素靶标（mTOR）通路的参与。综上所述，这些发现提示DM激活内源性BDNF / TrkB介导的MAPK和mTOR途径，从而增加神经突的生长。关键词：BDNF，溴氰菊酯，MAPK，mTOR，神经突的生长。表明有丝分裂原激活的蛋白激酶（MAPK）和哺乳动物雷帕霉素靶标（mTOR）通路的参与。综上所述，这些发现表明DM激活内源性BDNF / TrkB介导的MAPK和mTOR途径，从而增加了神经突的生长。关键词：BDNF，溴氰菊酯，MAPK，mTOR，神经突的生长。