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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Department of Biology, Indiana University-Purdue University, School of Science at Indianapolis, Indiana 46223.

Clin Exp Pharmacol Physiol. 1987 Apr;14(4):273-81. doi: 10.1111/j.1440-1681.1987.tb00972.x.

Drugs can be identified that relieve clinical symptoms of demyelinating diseases such as multiple sclerosis based on their ability to alter voltage-dependent ion channels in membranes and restore conduction in demyelinated nerve. Beneficial drugs either slow inactivation of membrane Na+ channels or block K+ channels. 2. Amantadine, an antiviral drug that slows Na+ inactivation in Myxicola giant axons, restores conduction in frog and rat sciatic nerves partially demyelinated by disruption of the perineurium (the 'perineurial window') loose ligatures, or lysolecithin. 3. A positive effect of amantadine on several different animal models supports the need for clinically oriented studies of amantadine and related inactivation-blocking agents in diseases such as multiple sclerosis.

基于药物改变膜上电压依赖性离子通道以及恢复脱髓鞘神经传导的能力，可以鉴别出能够缓解诸如多发性硬化症等脱髓鞘疾病临床症状的药物。有益的药物要么减缓膜Na⁺通道的失活，要么阻断K⁺通道。2. 金刚烷胺是一种抗病毒药物，可减缓巨型粘液虫轴突中Na⁺的失活，能使因破坏神经束膜（“神经束膜窗”）、松结扎线或溶血卵磷脂而部分脱髓鞘的青蛙和大鼠坐骨神经恢复传导。3. 金刚烷胺在几种不同动物模型上的积极作用，表明有必要针对金刚烷胺及相关失活阻断剂在诸如多发性硬化症等疾病中开展临床导向研究。

Department of Biology, Indiana University-Purdue University, School of Science at Indianapolis, Indiana 46223.

Clin Exp Pharmacol Physiol. 1987 Apr;14(4):273-81. doi: 10.1111/j.1440-1681.1987.tb00972.x.

Drugs can be identified that relieve clinical symptoms of demyelinating diseases such as multiple sclerosis based on their ability to alter voltage-dependent ion channels in membranes and restore conduction in demyelinated nerve. Beneficial drugs either slow inactivation of membrane Na+ channels or block K+ channels. 2. Amantadine, an antiviral drug that slows Na+ inactivation in Myxicola giant axons, restores conduction in frog and rat sciatic nerves partially demyelinated by disruption of the perineurium (the 'perineurial window') loose ligatures, or lysolecithin. 3. A positive effect of amantadine on several different animal models supports the need for clinically oriented studies of amantadine and related inactivation-blocking agents in diseases such as multiple sclerosis.

基于药物改变膜上电压依赖性离子通道以及恢复脱髓鞘神经传导的能力，可以鉴别出能够缓解诸如多发性硬化症等脱髓鞘疾病临床症状的药物。有益的药物要么减缓膜Na⁺通道的失活，要么阻断K⁺通道。2. 金刚烷胺是一种抗病毒药物，可减缓巨型粘液虫轴突中Na⁺的失活，能使因破坏神经束膜（“神经束膜窗”）、松结扎线或溶血卵磷脂而部分脱髓鞘的青蛙和大鼠坐骨神经恢复传导。3. 金刚烷胺在几种不同动物模型上的积极作用，表明有必要针对金刚烷胺及相关失活阻断剂在诸如多发性硬化症等疾病中开展临床导向研究。