Li C, Trapp B, Ludwin S, Peterson A, Roder J
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada.
J Neurosci Res. 1998 Jan 15;51(2):210-7. doi: 10.1002/(SICI)1097-4547(19980115)51:2<210::AID-JNR9>3.0.CO;2-G.
Myelin-associated glycoprotein (MAG) was postulated to play an important role in myelination. However, we showed previously that MAG null mutants exhibited no gross abnormality in myelination. Ultrastructural studies revealed subtle alterations in periaxonal organisation, indicating a restricted structural role for MAG in the formation and maintenance of periaxonal structures (Li et al., 1994). Here we show that myelination in MAG deficient mice is not as finely controlled as it is in wild type mice. The abnormalities manifest themselves as a decrease in the proportion of myelinated axons and a reciprocal increase in the proportion of unmyelinated axons in mutants' optic nerves. In addition, dysregulated myelination is occasionally observed in the form of multiply myelinated fibres, grouping of myelinated axons and myelin debris by a large myelin sheath, redundant myelin loops and, very rarely, massive myelin surrounding relatively small axons. Thus, in the absence of MAG, some glial cells seem unable to determine when, where and how much myelin should be laid down. These data support the notion of MAG being a glial recognition/adhesion molecule. A model is proposed regarding the roles MAG could play in the formation and maintenance of myelin structure.
髓鞘相关糖蛋白（MAG）被推测在髓鞘形成过程中发挥重要作用。然而，我们先前的研究表明，MAG基因敲除突变体在髓鞘形成方面未表现出明显异常。超微结构研究揭示了轴突周围组织的细微改变，表明MAG在轴突周围结构的形成和维持中具有有限的结构作用（Li等人，1994年）。在此，我们表明，MAG缺陷小鼠的髓鞘形成不像野生型小鼠那样受到精细调控。这些异常表现为突变体视神经中髓鞘化轴突比例的降低以及无髓鞘轴突比例的相应增加。此外，偶尔会观察到髓鞘形成失调，表现为多重髓鞘化纤维、髓鞘化轴突的聚集以及被大的髓鞘包裹的髓鞘碎片、多余的髓鞘环，并且非常罕见的是，相对较小的轴突被大量髓鞘包围。因此，在缺乏MAG的情况下，一些神经胶质细胞似乎无法确定何时、何地以及铺设多少髓鞘。这些数据支持MAG作为神经胶质识别/粘附分子的观点。我们提出了一个关于MAG在髓鞘结构形成和维持中可能发挥作用的模型。
