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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Noradrenergic and serotonergic blockade inhibits BDNF mRNA activation following exercise and antidepressant.
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Noradrenergic and serotonergic blockade inhibits BDNF mRNA activation following exercise and antidepressant.

机译：运动和抗抑郁后，去甲肾上腺素能和5-羟色胺能阻滞抑制BDNF mRNA的激活。

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Antidepressants and physical exercise have been shown to increase the transcription of hippocampal brain-derived neurotrophic factor (BDNF). Much evidence regarding the initial actions of antidepressant medications as well as exercise leads to the hypothesis that noradrenergic (NE) and/or serotonergic (5-HT) activation is a key element in the BDNF transcriptional elevation common to both interventions. Currently, we used short-term beta-adrenergic, 5-HT(1A), or 5-HT(2A/C) receptor blockade to characterize the influence of NE and 5-HT systems on BDNF transcription during physical exercise and antidepressant treatment. In situ hybridization revealed that beta-adrenergic blockade significantly blunted the BDNF mRNA elevations due to exercise, and also inhibited the modest elevations in the CA3 and dentate gyrus following short-term treatment with tranylcypromine. In contrast, 5-HT(2A/C) blockade only minimally altered exercise-induced BDNF mRNA levels, but inhibited up-regulation of BDNF transcription viatranylcypromine. Finally, 5-HT(1A) blockade did not inhibit exercise-induced BDNF mRNA elevations, but significantly enhanced levels above those achieved with exercise alone in the CA4. These results suggest that NE activation via beta-adrenergic receptors may be essential for both exercise and antidepressant-induced BDNF regulation. 5-HT(1A) and 5-HT(2A/C) activation, on the other hand, appear to be most important for antidepressant-induced BDNF regulation, but may also participate significantly in exercise-induced regulation in the CA4.
机译：抗抑郁药和体育锻炼已显示出可增加海马脑源性神经营养因子（BDNF）的转录。关于抗抑郁药以及运动的初始作用的许多证据导致这样一个假设，即去甲肾上腺素能（NE）和/或血清素能（5-HT）激活是两种干预措施共同导致的BDNF转录升高的关键因素。目前，我们使用短期β-肾上腺素，5-HT（1A）或5-HT（2A / C）受体阻滞来表征NE和5-HT系统对体育锻炼和抗抑郁治疗期间BDNF转录的影响。原位杂交显示，β-肾上腺素能阻断显着减弱了由于运动引起的BDNF mRNA升高，并且在用tranylcypromine短期治疗后还抑制了CA3和齿状回的适度升高。相比之下，5-HT（2A / C）只能最小程度地改变运动引起的BDNF mRNA水平，但可以抑制BDNF经由反式环丙胺的上调。最后，5-HT（1A）阻断剂不会抑制运动引起的BDNF mRNA升高，但是比CA4中单独运动所达到的水平显着提高。这些结果表明，通过β-肾上腺素能受体激活NE对于运动和抗抑郁药诱导的BDNF调节都是必不可少的。另一方面，5-HT（1A）和5-HT（2A / C）激活似乎是最重要的抗抑郁药诱导的BDNF调节，但也可能在CA4中显着参与运动诱导的调节。

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