Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Brain Res. 2010 Sep 10;1351:50-56. doi: 10.1016/j.brainres.2010.07.026. Epub 2010 Jul 15.
Multiple sclerosis (MS) patients may suffer from optic disturbances. Toxin-induced demyelinations have frequently been developed to investigate the cellular and structural aspects of demyelination and remyelination processes, separately. The present study describes functional consequence of lysolecithin (LPC)-induced lesion in the adult rat optic nerves and chiasm by recording the visual evoked potentials (VEPs) from the visual cortex and its correlation with myelin basic protein (MBP) expression in lesion site. Records of VEP were obtained at 2, 7, 14 and 28 days post-injection. We observed that the VEPs generated by light stimuli progressively changed in both amplitude and latency after the lesion as well as in comparison with those generated in control animals. These observations were confirmed through measurement of mRNA expression level for MBP which is one of the important genes expressed in mature oligodendrocytes and Schwann cells. The level of MBP mRNAs in demyelinated chiasm and optic nerves decreased following lysolecithin injection with its least value on day 7, and then it increased to the control level 14 days post-lesion. However, it continued to increase even after that and reached a maximum level 28 days post lesion. Results of the present paper show that, LPC injection in the chiasm share functional and molecular alterations which are found in demyelinating disorders in both the optic nerves and chiasm and also these alterations were coming back to level of control animal on 28 days post lesion, which is typically seen in myelin repair process. The present paper provides new insights into the experimental toxin-induced models that may be useful for evaluating the functional recovery of demyelinated optic nerves and chiasm following various repairing strategies. It also seems to be useful for studying the protective or remyelinating effects of different therapies in e.g. optic apparatus which is more affected by MS.
多发性硬化症 (MS) 患者可能会出现视神经障碍。毒素诱导的脱髓鞘已被广泛用于研究脱髓鞘和髓鞘再生过程的细胞和结构方面，分别进行研究。本研究通过记录从视皮层获得的视觉诱发电位 (VEPs) 并将其与病变部位髓鞘碱性蛋白 (MBP) 的表达相关联，描述了溶血卵磷脂 (LPC) 诱导的成年大鼠视神经和视交叉病变的功能后果。在注射后 2、7、14 和 28 天记录 VEP 记录。我们观察到，光刺激产生的 VEP 在病变后以及与对照动物相比，其幅度和潜伏期逐渐发生变化。通过测量 MBP 的 mRNA 表达水平证实了这些观察结果，MBP 是成熟少突胶质细胞和施万细胞中表达的重要基因之一。LPC 注射后，脱髓鞘视交叉和视神经中的 MBP mRNAs 水平下降，在第 7 天达到最低值，然后在损伤后 14 天增加到对照水平。然而，它继续增加，甚至在那之后达到最大值 28 天。本文的结果表明，LPC 注射到视交叉中会引起功能和分子改变，这些改变在视神经和视交叉的脱髓鞘疾病中都有发现，并且这些改变在损伤后 28 天会恢复到对照动物的水平，这是典型的髓鞘修复过程。本文为实验性毒素诱导模型提供了新的见解，这些模型可能有助于评估各种修复策略后脱髓鞘视神经和视交叉的功能恢复。对于研究例如视神经病变，这也可能对研究不同疗法的保护或髓鞘再生作用很有用，因为视神经病变在多发性硬化症中更为常见。
