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Open Access Cellular Compensatory Mechanisms in the CNS of Dysmyelinated Rats

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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.

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Document Type: Research Article

Affiliations: Department of Pathology and Molecular Medicine and Department of Surgery, McMaster University, Hamilton, Ontario, Canada. [email protected]

Publication date: 2010-06-01

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  • Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.

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