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We investigated whether in cultures of mechanically dissociated brain cells from newborn mice the reduction of the number of oligodendrocytes influences their proliferation rate. 14-day-old cultures were subjected to complement-dependent anti-galactocerebroside (GC) antibody-mediated cytotoxicity. The cytotoxic treatment completely destroyed oligodendrocytes. Thereafter, GC⁺ oligodendrocytes progressively reappeared. Their number was 20 and 66% compared to controls, 3 and 7 days after cytotoxicity, respectively. Proliferating oligodendrocytes were detected 3 and 7 days after cytotoxicity by combining the immunostaining for GC with ³H-thymidine autoradiography. The proliferation rate of oligodendrocytes in treated cultures was increased by 100 and 76% compared to controls, 3 and 7 days after cytotoxicity, respectively. These data suggest that the proliferation rate of oligodendrocytes can be influenced by extrinsic factors.

Sulfatide is enriched in the myelin sheath and accounts for 5% of the total lipids in this membrane. In the present work we describe the production and characterization of mouse monoclonal antibodies against sulfatide. The antibodies were detected and characterized in a previously described ELISA test system. The clone AIC3IA2 produced antibodies of the IgG3 class with high specificity for sulfatide. These antibodies showed almost no cross-reactivity with galactocerebroside or with any of the other lipids we tested. When used with the peroxidase antiperoxidase technique the antibodies stained a cell population either in fixed or unfixed brain cell cultures, indicating a surface localization of sulfatide in the respective cell population. In double-staining experiments the stained cell population was identified as myelin basic protein-positive oligodendrocytes.

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