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七鳃鳗网状脊髓轴突中的诱发性去极化和超极化电位

Evoked depolarizing and hyperpolarizing potentials in reticulospinal axons of lamprey.

作者信息

Matthews G, Wickelgren W O

出版信息

J Physiol. 1978 Jun;279:551-67. doi: 10.1113/jphysiol.1978.sp012361.

Abstract
  1. Intracellular recordings were made from reticulospinal axons (Müller axons) in the lamprey spinal cord. Electrical stimuli applied to the spinal cord surface elicited depolarizing and hyperpolarizing 'synaptic-like' potentials in Müller axons. The physiological basis of these evoked potentials was investigated. 2. The depolarizing response was not the result of increased extracellular K, as demonstrated by the constancy of the undershoot of the axonal action potential during the depolarization, by the failure of the response to summate during repetitive stimulation and by the failure of the response amplitude to vary as predicted when the [K] of the saline was varied. 3. When the membrane potential of the axon was varied by passing current through a micro-electrode, the amplitude of the depolarizing evoked potential decreased at membrane potentials positive to the resting potential and increased up to a maximum when the axon was hyperpolarized by about 10 mV. The extrapolated 'reversal potential' for the depolarizing response was about 15 mV positive to the normal -80 mV resting potential of the axon. However, the amplitude of the response did not continue to grow with hyperpolarizations greater than 10 mV, and, thus, the response did not behave as would a normal depolarizing synaptic potential. 4. Müller axons make numerous electrical synapses with spinal motoneurones and interneurones, and this suggested that the depolarizing response might be a coupling potential. In agreement with this idea, quantitative correspondence was found between changes in the input resistance of the axon produced by the depolarizing response and the variation in the depolarizing response amplitude. Thus, although the depolarizing response mimicked in some ways the behaviour of an excitatory synaptic potential, we conclude that it is a coupling potential. 5. The hyperpolarizing response also appeared to be a coupling potential. Its amplitude was not changed by hyperpolarizing the axon up to 30 mV and was decreased by depolarizing the axon sufficiently to decrease the axon's input resistance. 6. It is proposed that both depolarizing and hyperpolarizing evoked potentials in lamprey Müller axons are a result of passive flow of current from cells activated by the spinal cord stimulus and electrically coupled to Müller axons.
摘要
  1. 从七鳃鳗脊髓中的网状脊髓轴突(米勒轴突)进行细胞内记录。施加于脊髓表面的电刺激在米勒轴突中引发去极化和超极化的“类突触”电位。对这些诱发电位的生理基础进行了研究。2. 去极化反应不是细胞外钾离子增加的结果,这可通过去极化期间轴突动作电位负后电位的恒定、重复刺激期间反应不能总和以及当盐溶液中[K]变化时反应幅度未按预测变化来证明。3. 当通过微电极通电流改变轴突的膜电位时,去极化诱发电位的幅度在膜电位高于静息电位时降低,当轴突超极化约10 mV时增加至最大值。去极化反应的外推“反转电位”比轴突正常的 -80 mV静息电位正约15 mV。然而,当超极化大于10 mV时反应幅度并未继续增大,因此,该反应的表现与正常的去极化突触电位不同。4. 米勒轴突与脊髓运动神经元和中间神经元形成大量电突触,这表明去极化反应可能是一种耦合电位。与这一观点一致的是,在去极化反应引起的轴突输入电阻变化与去极化反应幅度变化之间发现了定量对应关系。因此,尽管去极化反应在某些方面模仿了兴奋性突触电位的行为,但我们得出结论,它是一种耦合电位。5. 超极化反应似乎也是一种耦合电位。将轴突超极化达30 mV时其幅度不变,而将轴突充分去极化以降低轴突输入电阻时其幅度减小。6. 有人提出,七鳃鳗米勒轴突中的去极化和超极化诱发电位都是由脊髓刺激激活并与米勒轴突电耦合的细胞的电流被动流动所致。

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