DNA, ganglioside and sulfatide in brains of rats given corticosterone in infancy, with an estimate of cell loss during development
| Autor: | Joyce A. Benjamins, Evelyn Howard |
|---|---|
| Rok vydání: | 1975 |
| Předmět: |
Male
medicine.medical_specialty Gestational Age Biology chemistry.chemical_compound Pregnancy Corticosterone Gangliosides Internal medicine medicine Neuropil Animals Humans Molecular Biology Brain Chemistry Sulfoglycosphingolipids Ganglioside DNA synthesis General Neuroscience Age Factors Brain DNA Embryonic stem cell Cell loss Rats Endocrinology medicine.anatomical_structure Animals Newborn chemistry Delayed-Action Preparations Immunology Sialic Acids RNA Female Neurology (clinical) Thymidine Developmental Biology |
| Zdroj: | Brain Research. 92:73-87 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/0006-8993(75)90528-4 |
| Popis: | Evidence of a postnatal loss of cerebral cells has been presented, based on counts of the activity of cerebral DNA following labeling with [3H]thymidine on embryonic day 14. In otherwise untreated rats, the loss was about 15 percent of the labeled cells between postnatal days 3 and 15. There was no further loss of activity thereafter. Littermates given corticosterone at day 3 showed little additional loss of labeled cells. Ganglioside NANA (N-acetylneuraminic acid) was reduced in proportion to the reduction in cerebral weight in the corticosterone treated rats. Sulfatide was reduced more, so that the concentration was 11 percent below that of the controls; It is concluded that the deficit in DNA after postnatal corticosterone treatment must be due primarily to an irreversible suppression of DNA synthesis, involving mainly glia. The reduction in gangliosides may represent a deficit in the growth of neuronal processes, leading to a reduction in the amount of neuropil, and perhaps contributing to a decrease in the number or size of myelinated axons. |
| Databáze: | OpenAIRE |
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