缺氧对猫和大鼠缓慢适应I型皮肤机械感受器的影响。

G S Findlater, E J Cooksey, A Anand, A S Paintal, A Iggo
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引用次数: 44

摘要

无论在什么哺乳动物受体系统中发现默克尔细胞,它们总是与一种典型的缓慢适应反应相关联。在缺氧环境下,通过对SAI受体及其传入纤维进行机械和电刺激,研究了Merkel细胞在大鼠和猫缓慢适应I型皮肤机械受体(SAI受体或触觉圆细胞)的转导过程中的作用。循环缺氧是通过给动物进行N2通气或肢体周围静脉血再循环而产生的。在这两种实验制剂中,得到的结果是相同的。对于受体失效的发生,我们发现肢体表面有一个缺氧的环境是必要的。这是通过将氮气注入放置在肢体上的气密聚乙烯袜子来实现的。不论动脉血PO2水平如何,将聚乙烯袜内的N2替换为O2足以使受体恢复。肢体周围N2刺激触觉穹隆时,受体反应与时间呈反比线性关系。相反,肢体周围的N2替换为O2后,反应随时间呈指数增长。与受体衰竭相关的是,通常在支配细胞的神经末梢附近的默克尔细胞细胞质中发现的致密囊泡数量显著减少。受体恢复与致密囊泡数量返回到对照细胞中发现的数量有关。缺氧对传入纤维中启动动作电位所需的电刺激水平没有影响,即使SAI受体对机械刺激的反应已经停止。结果表明,默克尔细胞致密囊泡是SAI机械感受器缓慢适应反应的必要条件,这可能是由于囊泡内储存的一种传递物质的分泌。
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The effects of hypoxia on slowly adapting type I (SAI) cutaneous mechanoreceptors in the cat and rat.

In whatever mammalian receptor system Merkel cells are found, they are always associated with a characteristic slowly adapting response. The role of Merkel cells in the transduction process of slowly adapting Type I cutaneous mechanoreceptors (SAI receptors or touch domes) of rats and cats was investigated by mechanical and electrical stimulation of SAI receptors and their afferent fibers in an O2-depleted environment. Circulatory hypoxia was produced either by ventilating animals with N2 or by recirculating venous blood around a limb. In both these experimental preparations, the results obtained were identical. For receptor failure to occur, it was found necessary to have an O2-depleted environment on the limb surface. This was achieved by passing N2 into a gas-tight polythene sock placed over the limb. Replacement of N2 within the polythene sock with O2 was sufficient to bring about receptor recovery, irrespective of arterial blood PO2 levels. There was an inverse linear relationship between receptor response and time when touch domes were stimulated with N2 around the limb. In contrast, the replacement of N2 around the limb with O2 produced an exponential increase in the response with time. Correlated with receptor failure was a significant reduction in the number of dense-cored vesicles normally found in the Merkel cell cytoplasm adjacent to the nerve ending innervating the cell. Receptor recovery was associated with a return in the number of dense-cored vesicles back to that found in control cells. Hypoxia had no effect on the level of electrical stimulation necessary to initiate an action potential in the afferent fiber, even though the response of SAI receptors to mechanical stimulation had ceased. The results indicate that Merkel cell dense-cored vesicles are necessary for the characteristic slowly adapting response of SAI mechanoreceptors and that this may be due to the secretion of a transmitter substance stored within the vesicles.

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