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Tachycardia evoked by disinhibition of the dorsomedial hypothalamus in rats is mediated through medullary raphe

机译:大鼠骨髓下丘脑被抑制引起的心动过速是由髓ra介导的

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摘要

Activation of neurons in the region of the dorsomedial hypothalamus (DMH) appears to generate the sympathetically mediated tachycardia seen in experimental stress in rats. The purpose of this study was to assess the role of neurons in the area of the medullary raphe pallidus (RP) in the tachycardia caused by stimulation of the DMH. The cardiovascular response to microinjection of the GABAA receptor antagonist bicuculline methiodide (BMI) 10 pmol (100 nl)−1 into the DMH was assessed before, and after, injection of the GABAA receptor agonist muscimol 80 pmol (100 nl)−1 or saline vehicle 100 nl into the RP in urethane-anaesthetized rats. Tachycardia evoked by microinjection of BMI into the DMH was mimicked by microinjection of BMI 30 pmol (75 nl)−1 into the RP. This DMH-induced tachycardia was markedly suppressed after injection of muscimol into the RP, but the response was unaffected by injection of saline into the same region. Thus, DMH-induced tachycardia is mediated through activation of neurons in the area of the RP, suggesting that these neurons may play a previously unrecognized role in stress-induced cardiac stimulation.
机译:在大鼠实验性应激中,背侧下丘脑(DMH)区域神经元的激活似乎产生了交感神经介导的心动过速。这项研究的目的是评估神经元在DMH刺激引起的心动过速中髓性睑裂(RP)区域中的作用。在将GABAA受体激动剂muscimol 80 pmol注射之前和之后,评估了GABAA受体拮抗剂拮抗双瓜氨酸甲硫氨酸(bMI)10 pmol(100 nl) -1 向DMH的心血管反应。在尿烷麻醉的大鼠中,将100 nl) -1 或盐水载体100 nl注入RP。将BMI微量注入DMH诱发的心动过速通过将30 pmol(75 nl) -1 的BMI微量注入来模拟。将muscimol注入RP后,该DMH诱导的心动过速得到明显抑制,但在同一区域注入生理盐水不会影响反应。因此,DMH诱导的心动过速是通过激活RP区域中的神经元来介导的,这表明这些神经元可能在应激诱导的心脏刺激中起着以前未被认识的作用。

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