PHYSIOLOGICAL CONSEQUENCES OF ANTISERUM-MEDIATED EXPERIMENTAL DEMYELINATION IN CNS
PHYSIOLOGICAL CONSEQUENCES OF ANTISERUM-MEDIATED EXPERIMENTAL DEMYELINATION IN CNS
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DOI：
10.1093/brain/111.3.675
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发表时间：
1988-06-01
期刊：
影响因子：
14.5
通讯作者：
SUMNER, AJ
中科院分区：
文献类型：
--
作者：
KAJI, R;SUZUMURA, A;SUMNER, AJ
为了研究免疫介导的中枢神经系统脱髓鞘的病理生理学机制，将20~30微升的多克隆抗半乳糖脑苷脂血清(AGC)注入20只Wistar大鼠的下胸段脊髓背柱。注射AGC的脊髓含有靠近注射部位轴突变性病灶的束状脱髓鞘区域。刺激胫神经后连续记录体感诱发电位。在注射AGC的动物中，85%的动物在注射后3天观察到以下特征：(1)皮层产生的电位波幅降低(P15)；(2)高频(50 Hz)脉冲的传递失败(率依赖性阻断)；(3)复合动作电位通过损毁部位的传导速度延迟。在注射生理盐水或对照兔血清的20只大鼠中，90%的大鼠没有看到这些变化。在7只丙烯酰胺诱导的轴索病变或沃勒氏变性大鼠中，未观察到速度依赖性阻滞。在注射AGC的大鼠中，临床症状(后肢共济失调)的出现与速率依赖性阻滞的发展最相关。在P15波幅恢复的同时，观察到注射后14天的临床恢复情况，此时率依赖的传导阻滞和降低的传导速度不变。3只大鼠高频传导恢复时间明显晚于临床恢复时间。这些发现表明，高频脉冲传递的失败可能会产生临床症状，对重新调整的脉冲序列的中枢适应机制在中枢神经系统脱髓鞘的临床恢复中发挥了作用。
To study the pathophysiology of immunologically mediated demyelination in the central nervous system (CNS), we inejcted 20 to 30 .mu.l of polyclonal antigalactocerebroside serum (AGC) into the lower thoracic dorsal column of the spinal cord in 20 Wistar rats. AGC-injected spinal cords contained areas of fascicular demyelination adjacent to the focus of axonal degeneration at the injection site. Somatosensory evoked potentials were recorded serially after tibial nerve stimulation. In 85% of AGC-injected animals, the following characteristics were observed by 3 days after injection: (1) decreased amplitude of the cortically generated potential (P15); (2) failure of transmission of high-frequency (50 Hz) impulses (rate-dependent block); (3) delayed conduction velocity of the compound action potentials through the lesion. None of these changes were seen in 90% of 20 rats injected with normal saline or control rabbit sera. In 7 rats with acrylamide-induced axonopathy or wallerian degeneration, the rate-dependent block was not observed. The onset of clinical symptoms (hindlimb ataxia) in AGC-injected rats was best correlated with development of the rate-dependent block. Clinical recovery was observed by 14 days after injection concurrent with restoration of P15 amplitude, when the rate-dependent block and decreased conduction velocities were unchanged. High-frequency-resistant conduction was re-established much later than clinical recovery in 3 rats. These findings suggest that failure of high-frequency impuse transmission may produce clinical symptoms and that a central adaptive mechanism to remodulated trains of impulses plays a role in clinical recovery from CNS demyelination.