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An electrophysiological study of the effects of atropine and physostigmine on transmission to the guinea-pig vas deferens

机译:阿托品和毒扁豆碱对豚鼠输精管传播的影响的电生理研究

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摘要

1. The effects of physostigmine and atropine on transmission to the longitudinal musculature of in vitro preparations of the guinea-pig vas deferens have been examined using intracellular micro-electrodes.2. Atropine (5 × 10-7 to 10-6 g/ml.) increased the rate of decay of excitatory junction potentials (EJPs) in response to post-ganglionic stimulation.3. Physostigmine (5 × 10-6 g/ml.) reduced the mean resting potential of the muscle cells from -60·5 to -51·5 mV and lowered the voltage of post-ganglionic stimulation necessary for initiation of an action potential in the muscle. In some but not all of the cells studied the time course of the EJP was markedly prolonged.4. At concentrations which did not alter the response to post-ganglionic stimulation (5 × 10-7 to 10-6 g/ml.), physostigmine caused fully facilitated EJPs to appear with the first pulse of a preganglionic train of stimulation.5. Atropine antagonized all the above effects of physostigmine.6. Physostigmine (5 × 10-7 to 10-6 g/ml.) also lowered the voltage of preganglionic stimulation necessary for initiation of an action potential in the muscle. This effect was not antagonized by atropine.7. The results are interpreted as being evidence for the existence of separate cholinergic and adrenergic motor fibres to the musculature of the guinea-pig vas deferens.
机译:1.使用细胞内微电极检测了毒扁豆碱和阿托品对豚鼠输精管体外制剂向纵向肌肉的传递的影响。2。阿托品(5×10 -7 至10 -6 g / ml。)增加神经节后刺激对兴奋性连接电位(EJPs)的衰减速率。 3。毒扁豆碱(5×10 -6 g / ml。)将肌肉细胞的平均静息电位从-60·5降低到-51·5 mV,并降低了神经节后刺激所需的电压启动肌肉中的动作电位。在一些但不是全部研究的细胞中,EJP的时间进程明显延长。4。在不改变对神经节后刺激的响应的浓度(5×10 -7 至10 -6 g / ml)下,毒扁豆碱可导致完全促进的EJP出现。神经节前刺激序列的第一个脉冲5。阿托品拮抗了毒扁豆碱的上述所有作用。6。毒扁豆碱(5×10 -7 至10 -6 g / ml。)还降低了在神经中启动动作电位所需的神经节前刺激电压。阿托品没有拮抗这一作用。7。结果被解释为豚鼠输精管的肌肉组织存在单独的胆碱能和肾上腺素能运动纤维的证据。

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