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[青蛙神经元在缺血状态下的形态功能变化]

[Morpho-functional changes in the frog neurons in ischemia].

作者信息

Darinskiĭ Iu A

出版信息

Tsitologiia. 1982 Dec;24(12):1430-4.

PMID:6984248
Abstract

After the full spinal cord ishemia in the frog, motoneuron lose their ability to generate spike potentials to a testing stimulation in 30 minutes. The size and structure of these neurons do not differ from those in the control ones. The ten minute high frequency stimulation of motoneurons affected by ishemia results in deep pathologic structural changes. The neuron dimensions decrease, and numerous picnomorphical, dark and vaculized neurons appear. The full ishemia leads to pathologic changes in the neuron structure. However, the number of picnomorphical and dark neurons is considerably less than that after the high frequency activation. Following the 90 minute ishemia, no postsynaptic or spike potentials occur in motoneurons as a response to their stimulation.

摘要

青蛙全脊髓缺血后,运动神经元在30分钟内失去了对测试刺激产生动作电位的能力。这些神经元的大小和结构与对照神经元并无差异。对受缺血影响的运动神经元进行10分钟的高频刺激会导致深度病理性结构变化。神经元尺寸减小,出现大量形态微小、颜色深且有空泡的神经元。完全缺血会导致神经元结构发生病理性变化。然而,形态微小和颜色深的神经元数量远少于高频激活后的数量。缺血90分钟后,运动神经元受到刺激时不会产生突触后电位或动作电位。

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