Central command: control of cardiac sympathetic and vagal efferent nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals

Central command: control of cardiac sympathetic and vagal efferent nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals
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DOI:
10.1113/expphysiol.2011.057661
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发表时间:
2012-01-01
影响因子:
2.7
通讯作者:
Matsukawa, Kanji
Matsukawa, Kanji
中科院分区:
医学4区
文献类型:
--
作者:
Matsukawa, Kanji

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高级大脑中心的前馈控制(称为中央命令)在运动期间心血管系统的自主调节中起作用。在过去的20年里,我们实验室的工作人员使用前丘前乳头体去脑动物模型来确定参与中枢神经系统控制心脏自主流出和动脉压力反射功能的神经回路。与运动开始时迷走神经收缩导致心率增加的传统观点相反,中枢命令并没有减少心脏迷走神经传出神经活动,但确实允许心脏交感传出神经活动产生心脏加速度。此外,中枢指令诱发的主动脉压力感受器心率反射的抑制减弱了主动脉神经刺激引起的压力反射介导的心动过缓,进一步增加了运动开始时的心率。在中丘水平去大脑的动物中,自发运动活动和相关的心血管反应消失。这些结果表明,包括间脑尾侧和延伸到中脑吻侧的脑区可能在产生中央命令中发挥作用。将荷包牡丹碱微量注射到去大脑大鼠中脑腹侧被盖区,产生与运动神经放电同步的肾交感神经活动的持久重复激活。当利多卡因微量注射到腹侧被盖区时,自发运动活动和相关的心血管反应停止。从这些研究结果,我们得出结论,大脑皮层输出触发激活的神经回路内的尾侧大脑,包括腹侧被盖区,这导致中央命令,以增加心脏交感神经流出在发病时的运动在去大脑动物模型。
Feedforward control by higher brain centres (termed central command) plays a role in the autonomic regulation of the cardiovascular system during exercise. Over the past 20 years, workers in our laboratory have used the precollicularpremammillary decerebrate animal model to identify the neural circuitry involved in the CNS control of cardiac autonomic outflow and arterial baroreflex function. Contrary to the traditional idea that vagal withdrawal at the onset of exercise causes the increase in heart rate, central command did not decrease cardiac vagal efferent nerve activity but did allow cardiac sympathetic efferent nerve activity to produce cardiac acceleration. In addition, central command-evoked inhibition of the aortic baroreceptorheart rate reflex blunted the baroreflex-mediated bradycardia elicited by aortic nerve stimulation, further increasing the heart rate at the onset of exercise. Spontaneous motor activity and associated cardiovascular responses disappeared in animals decerebrated at the midcollicular level. These findings indicate that the brain region including the caudal diencephalon and extending to the rostral mesencephalon may play a role in generating central command. Bicuculline microinjected into the midbrain ventral tegmental area of decerebrate rats produced a long-lasting repetitive activation of renal sympathetic nerve activity that was synchronized with the motor nerve discharge. When lidocaine was microinjected into the ventral tegmental area, the spontaneous motor activity and associated cardiovascular responses ceased. From these findings, we conclude that cerebral cortical outputs trigger activation of neural circuits within the caudal brain, including the ventral tegmental area, which causes central command to augment cardiac sympathetic outflow at the onset of exercise in decerebrate animal models.