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急性暴露于抗半乳糖脑苷脂血清后大鼠有髓纤维的传导阻滞

Conduction block in rat myelinated fibres following acute exposure to anti-galactocerebroside serum.

作者信息

Lafontaine S, Rasminsky M, Saida T, Sumner A J

出版信息

J Physiol. 1982 Feb;323:287-306. doi: 10.1113/jphysiol.1982.sp014073.

DOI:10.1113/jphysiol.1982.sp014073
PMID:7097575
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1250357/
Abstract
  1. We have observed conduction in single rat spinal ventral root nerve fibres following acute topical application of anti-galactocerebroside serum.2. Conduction of nerve impulses was initially slowed and subsequently blocked at the site of serum exposure.3. Conduction block occurred within as little as 1 hr in more slowly conducting (20-30 m/sec) myelinated fibres but occurred later in fibres conducting more rapidly.4. Conduction block was preceded by a rise in internodal conduction time from the normal 20 musec to about 200 musec.5. At nodes exposed to serum, conduction block was invariably associated with greatly decreased depolarization; this was contrasted with nodes exposed to local anaesthetic or tetrodotoxin where conduction block occurred despite nodal depolarization well beyond threshold potential.6. Nodal capacitance and resistance were estimated from simultaneous recordings of membrane current and extracellular potential at blocked nodes exposed to local anaesthetic or tetrodotoxin (normal nodes) and at blocked nodes exposed to anti-galactocerebroside serum.7. For normal fibres of internodal length 0.8-1.1 mm, an upper limit estimate for average nodal capacitance was 2.6 +/- 0.3 pF and a lower limit estimate for average nodal resistance was 55 +/- 10 MOmega. There was an order of magnitude increase in the capacitance of nodes at which conduction block occurred following exposure to anti-galactocerebroside serum.8. We conclude that the early conduction block caused by anti-galactocerebroside serum is due to paranodal demyelination and that acute paranodal demyelination is sufficient to cause conduction block.
摘要
  1. 在急性局部应用抗半乳糖脑苷脂血清后,我们观察到了单个大鼠脊髓腹根神经纤维中的传导情况。

  2. 神经冲动的传导最初减慢,随后在血清接触部位被阻断。

  3. 在传导较慢(20 - 30米/秒)的有髓纤维中,传导阻断在短短1小时内就会发生,但在传导较快的纤维中则出现得较晚。

  4. 传导阻断之前,节间传导时间从正常的20微秒增加到约200微秒。

  5. 在暴露于血清的节段,传导阻断总是与去极化显著降低相关;这与暴露于局部麻醉剂或河豚毒素的节段形成对比,在后者中,尽管节段去极化远超阈电位,但仍会发生传导阻断。

  6. 通过同时记录暴露于局部麻醉剂或河豚毒素(正常节段)的阻断节段以及暴露于抗半乳糖脑苷脂血清的阻断节段的膜电流和细胞外电位,来估计节段电容和电阻。

  7. 对于节间长度为0.8 - 1.1毫米的正常纤维,平均节段电容的上限估计为2.6 +/- 0.3皮法,平均节段电阻的下限估计为55 +/- 欧姆。暴露于抗半乳糖脑苷脂血清后发生传导阻断的节段的电容增加了一个数量级。

  8. 我们得出结论:抗半乳糖脑苷脂血清引起的早期传导阻断是由于结旁脱髓鞘,并且急性结旁脱髓鞘足以导致传导阻断。

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本文引用的文献

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