RESTORATION OF BLOOD-NERVE BARRIER IN NEUROPATHY IS ASSOCIATED WITH AXONAL REGENERATION AND REMYELINATION
RESTORATION OF BLOOD-NERVE BARRIER IN NEUROPATHY IS ASSOCIATED WITH AXONAL REGENERATION AND REMYELINATION
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DOI：
10.1097/00005072-199111000-00004
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发表时间：
1991-11-01
影响因子：
3.2
通讯作者：
GOINES, ND
中科院分区：
文献类型：
--
作者：
BOULDIN, TW;EARNHARDT, TS;GOINES, ND
我们研究了在神经横断或神经挤压后的碲神经病变、蓖麻神经病变和沃勒氏变性的演变过程中血神经屏障（BNB）破坏的时间过程。在神经病变发生后3天至19周，用4000分子量荧光右旋糖酐评估血神经屏障的通透性。所有四种神经病变模型在前两周均出现血神经屏障破坏。在以快速髓鞘再生为特征的脱髓鞘神经病变模型tellurium神经病和以快速轴突再生为特征的Wallerian变性神经损伤模型中，BNB在四周内开始恢复到右旋糖酐，并在14周内完成。相比之下，蓖麻毒素神经病（一种没有轴突再生或髓鞘再生的神经病模型）和神经横断后的沃勒氏变性模型（以极少量轴突再生到远端残端为特征）的BNB破坏持续超过14周。我们从这些数据中得出结论，在不同类型的神经病变过程中，BNB的改变是不同的，这些改变依赖于神经纤维损伤的形式。蓖麻毒素神经病和神经横断后缺乏再生或再髓鞘轴突可能是这些神经病中发现的持续BNB破坏的原因。
We investigated the temporal course of blood-nerve barrier (BNB) breakdown during the evolution of tellurium neuropathy, ricin neuropathy, and Wallerian degeneration following nerve transection or nerve crush. Blood-nerve barrier permeability was assessed with a 4,000-molecular weight fluoresceinated dextran from three days to 19 weeks after onset of neuropathy. Blood-nerve barrier breakdown was present during the first two weeks in all four models of neuropathy. Restoration of the BNB to the dextran began within four weeks and was complete by 14 weeks in tellurium neuropathy, a model of demyelinating neuropathy characterized by rapid remyelination, and after nerve crush, a model of Wallerian degeneration characterized by rapid axonal regeneration into distal stump. In contrast, there was persistence of BNB breakdown beyond 14 weeks in ricin neuropathy, a model of neuropathy with no axonal regeneration or remyelination, and after nerve transection, a model of Wallerian degeneration characterized by minimal axonal regeneration into distal stump. We conclude from these data that alterations in the BNB over the course of neuropathy differ among various types of neuropathy, and that these alterations are dependent on the form of nerve fiber injury. The lack of regenerating or remyelinating axons in ricin neuropathy and after nerve transection may be responsible for the persistent BNB breakdown found in these neuropathies.