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首页> 外文期刊>The European Journal of Neuroscience >Hippocampal activation of 5-HT1B receptors and BDNF production by vagus nerve stimulation in rats under chronic restraint stress
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Hippocampal activation of 5-HT1B receptors and BDNF production by vagus nerve stimulation in rats under chronic restraint stress

机译:在慢性约束压力下大鼠迷走神经刺激的5-HT1B受体和BDNF产生的海马活化

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A growing body of evidence shows that the electrical stimulation of the vagus nerve can improve mental illness including depression. Here, we investigated whether the vagus nerve stimulation (VNS) is involved in regulating the responsiveness of hippocampal neurons in rats under chronic restraint stress (CRS). c-Fos protein signals were detected 2 hr after VNS in 5-HT1A receptor-positive neurons in the dorsal raphe nucleus (DRN) as well as in the nucleus tractus solitarius (NTS). Chronic VNS was performed on a daily basis for 2 weeks using an implanted microelectrode in rats that had undergone CRS for 2 weeks. We found that the levels of both 5-HT1B receptors and phospho-Erk1/2 were decreased in parallel in the hippocampal neurons of CRS animals and then increased to the baseline levels by chronic VNS. Hippocampal induction of 5-HT1B receptors and phospho-Erk1/2 by VNS was diminished after the injection of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin of serotonergic neurons, into the DRN. Hippocampal production of brain-derived neurotrophic factor (BDNF) was also upregulated by VNS, but the treatment of 5,7-DHT abrogated the effects of VNS on BDNF induction. VNS in CRS animals improved the behavioral scores in forced swimming test (FST) compared to sham-stimulated control. Our results suggest that VNS-mediated serotonergic input via 5-HT1B receptors into the hippocampal neurons may activate BDNF pathway and improve depressive-like behaviors in CRS animals.
机译:越来越多的证据表明,迷走神经的电刺激可以改善包括抑郁症的精神疾病。在这里,我们研究了迷走神经刺激(VNS)是否参与调节慢性约束应激(CRS)下大鼠大鼠的海马神经元的反应性。在压甲核(DRN)中的5-HT1A受体阳性神经元中的VNS之后检测到C-FOS蛋白信号2小时,以及核泌尿菌菌(NTS)。每天进行慢性VN,每天使用植入的微电极在经过CRS 2周内的大鼠中进行2周。我们发现,在CRS动物的海马神经元中,5-HT1B受体和磷酸-ERK1 / 2的水平在CRS动物的海马神经元平行下降,然后通过慢性VNS增加到基线水平。在注射5,7-二羟基对胺(5,7-DHT),血清酮神经元的神经毒素,进入DRN后,VNS的海马诱导5-HT1B受体和磷酸-ERK1 / 2在DRN中减少。脑衍生的神经营养因子(BDNF)的海马产量也受VNS上调,但5,7-DHT的治疗废除了VNS对BDNF诱导的影响。与假刺激的控制相比,CRS动物中的VNS在强制游泳测试(FST)中改善了行为分数。我们的研究结果表明,VNS介导通过5-HT1B受体进入海马神经元的血清奈莫酮,可以激活BDNF途径,并改善CRS动物中的抑郁样行为。

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