脱髓鞘大鼠中枢神经系统中的细胞代偿机制。
Cellular compensatory mechanisms in the CNS of dysmyelinated rats.
作者信息
Kwiecien Jacek M
机构信息
Department of Pathology and Molecular Medicine and Department of Surgery, McMaster University, Hamilton, Ontario, Canada.
出版信息
Comp Med. 2010 Jun;60(3):205-17.
Loss or absolute lack of myelin in the CNS results in remarkable compensation at the cellular level. In this study on the natural progression of neuropathology in the CNS in 2 related but distinct long-lived dysmyelinated rats, total lack of myelin was associated with remarkable glial cell proliferation and ineffective myelinating activity throughout life in Long Evans Bouncer (LE-bo) rats; conversely, in Long Evans Shaker (LES) rats, futile myelinating activity ceased when rats were advanced in age. Progressively severe astrogliosis separates individual axons from each other and coincides with widespread, abundant axonal sprouting throughout the life in both rat strains. Severely dysmyelinated Long Evans rats can serve as excellent models to elucidate the cellular and molecular mechanisms of neuroglial compensation to lack or loss of myelin in vivo and to study axonal plasticity in the adult demyelinated CNS.
中枢神经系统（CNS）中髓磷脂的缺失或完全缺乏会在细胞水平上导致显著的代偿。在这项关于两种相关但不同的长寿脱髓鞘大鼠中枢神经系统神经病理学自然进展的研究中，完全缺乏髓磷脂与朗-伊文斯弹跳鼠（LE-bo）终生显著的胶质细胞增殖和无效的髓鞘形成活动相关；相反，在朗-伊文斯颤抖鼠（LES）中，当大鼠年龄增长时，无效的髓鞘形成活动停止。逐渐严重的星形胶质细胞增生将单个轴突彼此分开，并且在两种大鼠品系的整个生命过程中都与广泛、丰富的轴突发芽同时出现。严重脱髓鞘的朗-伊文斯大鼠可作为优秀的模型，用于阐明体内神经胶质细胞对髓磷脂缺乏或缺失的代偿的细胞和分子机制，以及研究成年脱髓鞘中枢神经系统中的轴突可塑性。
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