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CTB-saporin induced demyelinating myelopathy in the rat.

Janni G, Lappi DA, Ohara PT, Jasmin L (1999) CTB-saporin induced demyelinating myelopathy in the rat. Neuroscience 1999 Abstracts 731.2. Society for Neuroscience, Miami, FL.

Summary: In designing a rat model of demyelinating disease, we have used a newly developed neurotoxin, the B fragment of cholera toxin (CTB) linked to the potent ribosome inactivating protein saporin. Saporin linked to CTB targets cell expressing ganglioside GM1 on their surface, mainly Schwann cells, oligodendrocytes, and to a lesser degree neurons. After binding to GM1, CTB-Saporin is rapidly endocytosed and induces cell death. We demonstrate that intrathecal injection of 1 µg in 5 µl of CTB-Saporin at the lumbar level produces a demyelinating disease of the spinal cord. Behaviorally, this disease is characterized by an ascending paralysis that progresses most prominently from day 7 to day 14 post-treatment. In approximately half of the animals, the disease progresses to the brainstem, while in the others the disease regresses spontaneously, leaving these animals with only a moderate residual neurologic deficit. Histologically and ultrastructurally, the spinal pathology is characterized by a loss of myelin and oligodendroglyocytes as well as an immune response involving circulating leukocytes. Immunostaining shows the presence of CD8 immunopositive T lymphocytes but not CD4 T lymphocytes. We therefore conclude that CTB-Saporin induced demyelination involves an immune, but not an autoimmune mediated component in addition to the direct cytotoxic effect. Supported by Georgetown University.

Related Products: CTB-SAP (Cat. #IT-14)

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