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Input-output relationships of central neural circuits involved in respiration in cats

机译:与猫呼吸有关的中枢神经回路的输入输出关系

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摘要

1. Inspiratory output responses, measured as integrated phrenic activity, to hypercapnia, to unilateral and bilateral carotid sinus nerve stimulation and to combinations of these stimuli were determined in paralysed, vagotomized and glomectomized cats whose end-tidal PCO2 was kept constant by means of a servo-controlled ventilator. In addition, the effect on these responses of the mechanism that causes the respiratory after-discharge was determined.2. Above the threshold for rhythmic activity, the inspiratory response to hypercapnic stimulation of the central chemoreceptor was curvilinear, showing progressively smaller increments of output for equal increments of PCO2 as the latter became higher.3. The combining of stimuli from right and left carotid sinus nerves failed to show an algebraically additive effect; the response was approximately 70% of that predicted from a summing of the separate stimuli given alone.4. The response to a constant carotid sinus nerve test stimulus was progressively decreased in magnitude as the pre-stimulus level of respiratory activity was increased by conditioning stimulation of the central chemoreceptors by hypercapnia, by stimulation of the opposite carotid sinus nerve or by the mechanism that generates an after-discharge.5. From a descriptive standpoint, our findings show that there is a negative or hypoadditive interaction between the peripheral and central inputs at the level of the central respiratory controller. However, we present evidence that, rather than being a specific interaction between peripheral and central inputs, the response is due to the properties of a neural component of the central pathway. This component is common to both inputs and develops progressive saturation of its neural elements as its activity increases.6. In addition, the neural mechanism which generates a respiratory after-discharge appears to saturate completely at a lower level of inspiratory activity than that at which the common pathway develops complete saturation. This finding supports the idea that this mechanism represents an independent input to the respiratory controller.7. Because the described a-linear response characteristics of the central respiratory controller are due to its inherent neuronal properties rather than to specific interactions between inputs, we suggest that studies of such `interactions' must be interpreted with this consideration in mind.
机译:1.通过瘫痪,迷走神经切断术和角膜切除术的猫确定呼气末输出的反应,以综合活动,对高碳酸血症,对单侧和双侧颈窦神经刺激以及对这些刺激的组合的影响,通过潮气使PCO2保持恒定伺服控制呼吸机。此外,确定了引起呼吸后放电的机制对这些反应的影响。2。在节律活动阈值以上,中央化学感受器对高碳酸血症刺激的吸气反应呈曲线,显示出输出的增量逐渐减小,而PCO2则随着PCO2的增加而逐渐增加。3。左右颈动脉窦神经的刺激结合没有表现出代数加和作用;响应约为单独给予单独刺激的总和所预测的响应的70%。4。随着高碳酸血症对中央化学感受器的刺激,对侧颈动脉窦神经的刺激或产生机制,对恒定颈动脉窦神经测试刺激的反应的幅度逐渐降低,因为刺激前呼吸活动的水平增加放电后5。从描述的角度来看,我们的发现表明,在中央呼吸控制器的水平上,外围输入和中央输入之间存在负或负加性交互作用。但是,我们提供的证据表明,响应不是中央和外围输入之间的特定交互作用,而是由于中央通路的神经成分的特性所致。该成分对于两种输入都是​​通用的,并且随着其活性的增加其神经元素逐渐饱和。6。另外,产生呼吸后放电的神经机制似乎在吸气活动水平比完全途径完全饱和的吸气活动水平完全饱和。这一发现支持了这种机制代表呼吸控制器的独立输入的想法7。因为所描述的中央呼吸控制器的a线性响应特性是由于其固有的神经元特性,而不是由于输入之间的特定交互作用,所以我们建议对此类“交互作用”的研究必须考虑到这一点。

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