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从豚鼠结肠带血管周围抑制神经向平滑肌的传递。

Transmission from perivascular inhibitory nerves to the smooth muscle of the guinea-pig taenia coli.

作者信息

Bennett M R, Burnstock G, Holman M E

出版信息

J Physiol. 1966 Feb;182(3):527-40. doi: 10.1113/jphysiol.1966.sp007835.

DOI:10.1113/jphysiol.1966.sp007835
PMID:5941664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1357485/
Abstract
  1. Membrane potential changes of the smooth muscle cells of the taenia coli were recorded during stimulation of the perivascular inhibitory nerves.2. Some spontaneous action potentials were preceded by a slow pacemaker-like potential. Others began at or near the maximum level of the membrane potential and were not preceded by pacemaker-like potentials.3. There were no changes in the membrane potential of smooth muscle cells when the inhibitory nerves were stimulated with a single pulse. Stimulation at frequencies greater than 5 pulses/sec caused a hyperpolarization of the smooth muscle membrane. This resulted in a decrease in spike frequency and relaxation.4. When the frequency of stimulation of the inhibitory nerves was increased there was an increase in the amplitude and rate of rise of the hyperpolarization and a decrease of the latency. The latency varied from 150 to 300 msec, and the largest hyperpolarization recorded was 16 mV.5. The effect of the hyperpolarization due to nerve stimulation in cells showing pacemaker-like activity was to increase the level of the membrane potential at which the action potentials began and to increase the membrane potential to which the action potentials repolarized. Action potentials which occurred during hyperpolarizations of the membrane had greater rates of rise and fall and larger amplitudes than did the action potentials which occurred before hyperpolarization.6. The effect of the hyperpolarization due to nerve stimulation in cells which did not show pacemaker-like activity depended on the amplitude of the hyperpolarization. Small hyperpolarizations exposed small depolarizations of the membrane which occurred when an action potential would normally have been expected. Large hyperpolarizations blocked the action potentials entirely.7. Action potentials did not begin firing again at the normal rate immediately after stimulation ceased. The time taken for the rate of firing of action potentials to return to normal increased with increasing frequency of stimulation.8. The hyperpolarization in response to perivascular inhibitory nerve stimulation was blocked by guanethidine and bretylium.
摘要
  1. 在刺激血管周围抑制神经期间,记录了结肠带平滑肌细胞的膜电位变化。

  2. 一些自发动作电位之前有一个缓慢的起搏器样电位。其他动作电位则在膜电位的最大水平或其附近开始,且之前没有起搏器样电位。

  3. 用单个脉冲刺激抑制神经时,平滑肌细胞的膜电位没有变化。以大于5次脉冲/秒的频率刺激会导致平滑肌膜超极化。这导致动作电位频率降低和松弛。

  4. 当抑制神经的刺激频率增加时,超极化的幅度和上升速率增加,潜伏期缩短。潜伏期从150到300毫秒不等,记录到的最大超极化是16毫伏。

  5. 神经刺激引起的超极化对表现出起搏器样活动的细胞的作用是提高动作电位开始时的膜电位水平,并提高动作电位复极化时的膜电位。在膜超极化期间发生的动作电位比超极化之前发生的动作电位具有更大的上升和下降速率以及更大的幅度。

  6. 神经刺激引起的超极化对未表现出起搏器样活动的细胞的作用取决于超极化的幅度。小的超极化暴露了在正常预期动作电位时发生的膜的小去极化。大的超极化完全阻断动作电位。

  7. 刺激停止后,动作电位不会立即以正常速率再次发放。动作电位发放速率恢复正常所需的时间随着刺激频率的增加而增加。

  8. 血管周围抑制神经刺激引起的超极化被胍乙啶和溴苄铵阻断。

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J Physiol. 1966 Feb;182(3):527-40. doi: 10.1113/jphysiol.1966.sp007835.
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