Deloire-Grassin M S, Brochet B, Quesson B, Delalande C, Dousset V, Canioni P, Petry K G
Neurobiologie des Affections de la Myéline, BP 78, CNRS, UMR5536, Université Victor Segalen, 146 rue Léo Saignat, 33076 Cedex, Bordeaux, France.
J Neurol Sci. 2000 Sep 1;178(1):10-6. doi: 10.1016/s0022-510x(00)00331-2.
The aim of this work was to assess quantitatively and qualitatively the ability of magnetization transfer imaging to follow in vivo remyelination. Demyelination lesions were induced in rats by the injection of L-alpha-lysophosphatidylcholine stearoyl into the corpus callosum and imaging was performed in vivo on a 4.7-Tesla system at different time points. The percentage of magnetization transfer ratio (MTR) decrease was calculated for each animal. To evaluate the MTR findings for remyelination, myelin was quantitated by histological analysis of the lesion size and counting the number of remyelinating axons. An MTR decrease was observed when demyelination was present at 7 days after injection. During the remyelinating phase between day 30 and 40 after injection, contralateral values almost complete returned to normal, thus indicating remyelination. Histologically, at days 30 and 40 after injection, the lesion area was reduced in size and the axons were surrounded by a thin myelin sheath, indicating the remyelination process. Statistical analysis showed that the profile of MTR values was significantly correlated with the course of remyelination. All the MTR changes show a correlation with both myelin damage and repair. In conclusion, the study of the MTR profile in this myelin lesion model demonstrates in vivo the loss of myelin and the presence of spontaneous remyelination. This methodological approach which can also be applied to multiple sclerosis patients to show demyelination, should prove helpful to determine the degree of spontaneous and therapeutically induced remyelination in multiple sclerosis lesions, and thus to validate therapeutic treatments for myelin repair.
这项工作的目的是定量和定性地评估磁化传递成像跟踪体内髓鞘再生的能力。通过向大鼠胼胝体注射L-α-溶血磷脂酰胆碱硬脂酰诱导脱髓鞘病变,并在4.7特斯拉系统上于不同时间点对大鼠进行活体成像。计算每只动物的磁化传递率(MTR)下降百分比。为了评估MTR在髓鞘再生方面的表现,通过对病变大小进行组织学分析并计数再髓鞘化轴突的数量来对髓磷脂进行定量。注射后7天出现脱髓鞘时观察到MTR下降。在注射后30至40天的再髓鞘化阶段,对侧值几乎完全恢复正常,从而表明发生了髓鞘再生。组织学上,注射后30天和40天,病变区域大小减小,轴突被薄的髓鞘包围,表明发生了髓鞘再生过程。统计分析表明,MTR值曲线与髓鞘再生过程显著相关。所有MTR变化均显示与髓鞘损伤和修复相关。总之,在这个髓鞘病变模型中对MTR曲线的研究在体内证明了髓鞘的丢失和自发髓鞘再生的存在。这种方法学方法也可应用于多发性硬化症患者以显示脱髓鞘,应该有助于确定多发性硬化症病变中自发和治疗诱导的髓鞘再生程度,从而验证髓鞘修复的治疗方法。