Gliotoxin에 의한 척수 뉴론의 손상이 운동유발전위에 미치는 영향

Abstract

Demyelinating lesions induced by intraspinal injecion of gliotoxin have been studied in order to gain insights into reasons for failure of remyelination and to improve understanding of the axonal conduction disorders such as multiple sclerosis. The present study was conducted to determine whether there is any change in central conduction during demyelination and subsequent remyelination of the dorsal funiculus of the rat spinal cord after injection of gliotoxin, and furthermore, whether intraperitoneal administration of mexiletine, an antiarrhythmic and Na+ channel blocker, has any effect on recovery from demyelination. Male Sprague-Dawley rats were anesthetized with pentobarbital. Ethidium bromide was injected into the dorsal funiculus of the thoracic spinal core (at the level of the 3rd thoracic vertebra; T3) of the rats to induce demylination. Some of these rats received intraperitoneal injection of mexiletine every day after surgery. After 14 postoperative (p.o.) days, the rats were reanesthetized and subjected to motor evoked potential (MEP) recording. MEPs were recorded from the bipolar disk electrode placed upon the surface of the spinal core at the level of the 6th thoracic vertebra (T6), while the contralateral motor cortex was stimulated by another disk electrode. There were two distinctively different negative and positive peaks in MEPs. Demyelination produced by gliotoxin resulted in conduction delay in MEPs. The rats received injection of mexiletine showed shortened MEP latencies compared to the rats which did not receive mexiletine. These results suggest that demyelination delays central conduction measured by MEPs and that systemic mexiletine may play a role in protecting neural tissues from demyelination.