期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1984
卷号：81
期号：18
页码：5638-5642
DOI：10.1073/pnas.81.18.5638
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Fetal cerebral neurons at the initiation of active neurite outgrowth in culture incorporate 4-fold more [3H]glucosamine into glycoproteins than into the cellular lipid fraction. After 8 days or longer, when a well-developed fiber network is apparent, lipids are labeled more extensively than the glycoproteins. Labeling of the latter is inhibited 95% and 89% by 0.5 microgram of tunicamycin per ml added to 1-day-old and 8-day-old cultures, respectively. Labeling of glycolipids is inhibited 30% in 1-day-old and 86% in 8-day-old cultures. Tunicamycin blocks incorporation of glucosamine label into practically all ganglioside species except for a resorcinol-positive, sialidase-sensitive band tentatively identified as GQ1b tetrasialoganglioside (Svennerholm ganglioside nomenclature). It also substantially reduces binding of 125I-labeled tetanus toxin to intact cells. There is 14% and 27% reduction in the total ganglioside sialic acid content in 1-day-old and 8-day-old cells treated for 24 hr with 0.5 microgram of tunicamycin per ml, but no substantial compositional changes are encountered. Tunicamycin blocks neurite outgrowth when added to cells soon after plating but causes no retraction or losses of fibers once the fiber network is established. Therefore, inhibition of neurite outgrowth by tunicamycin is not due to an effect on cellular gangliosides but can be correlated to an inhibition of protein glycosylation.
