首页> 美国卫生研究院文献>The Journal of Physiology >Prolonged changes in excitability of pyramidal tract neurones in the cat: a post-synaptic mechanism.
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Prolonged changes in excitability of pyramidal tract neurones in the cat: a post-synaptic mechanism.

机译:在猫的锥体束神经元的兴奋性的长期变化:突触后的机制。

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摘要

1. Prolonged changes in the excitability of cortical neurones can be produced by altering their firing rates for brief periods. In the anaesthetized cat, increased firing of pyramidal tract cells induced by trains of antidromic conditioning shocks led to increases in cell excitability, as measured by the size of the mass response at the medullary pyramid to test shocks applied to the cortical surface. We have shown in two ways that post-synaptic mechanisms could be responsible. 2. In one experimental design, MgCl2 solution (1 mole/l.) was applied to the cortical surface in order to block synaptic activity throughout the cortical depth. Following antidromic conditioning trains, cell excitability was increased; the size of the mass response was up to 30% larger than the control values. This persisted undiminished for up to 3 hr. 3. In the second experimental design, synaptic activity was not blocked, but we compared the effects of antidromic plus synaptic activation of pyramidal tract cells with the effects of synaptic activation alone. Antidromic plus synaptic activation was obtained by applying conditioning trains to the pyramidal tract at the medulla ipsilateral to the cortical test shock; prolonged increases in the ipsilateral response to the test shock were produced. Synaptic activation alone was obtained by the same conditioning trains, but in those cells whose axons projected into the contralateral pyramidal tract; prolonged increases in the contralateral response to the cortical test shock were never seen. In many instances prolonged decreases in excitability were found. 4. We conclude that prolonged increases in excitability of pyramidal tract cells can occur in the absence of any synaptic input, demonstrating that the underlying mechanism is post-synaptic; this does not preclude the action of synaptic mechanisms when synaptic transmission is not blocked.
机译:1.短暂改变皮层神经元的放电速率可引起皮质神经元兴奋性的长期变化。在麻醉的猫中,由一系列抗病态条件性休克引起的锥体束细胞的发射增加,导致细胞兴奋性增加,这是通过髓质金字塔的质量响应大小来测试的,以测试施加于皮质表面的休克。我们以两种方式表明了突触后机制可能是负责任的。 2.在一项实验设计中,将MgCl2溶液(1摩尔/升)应用于皮质表面,以阻止整个皮质深度的突触活性。进行抗病态调节后,细胞兴奋性增加;质量响应的大小比对照值大30%。这种情况持续了3个小时。 3.在第二个实验设计中,突触活性没有被阻止,但是我们将锥体束的抗drodroplus突触激活的效果与单独的突触激活的效果进行了比较。通过在皮质测试电击的同侧延髓的锥体束上施加条件调节序列,获得抗皮肤加突触激活。导致同侧对测试电击的反应时间延长。单独的突触激活是通过相同的条件训练获得的,但是在那些轴突伸入对侧锥体束的细胞中。从未观察到对皮层试验休克的对侧反应持续时间延长。在许多情况下,发现兴奋性长期下降。 4.我们得出的结论是,在没有任何突触输入的情况下,锥体束细胞的兴奋性可能会延长,这表明潜在的机制是突触后。当突触传递未被阻断时,这并不排除突触机制的作用。

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