Effects of Abnormal Thyroid State and Undernutrition on Carbonic Anhydrase and Oligodendroglia Development in the Rat Cerebellum
- 1 January 1982
- journal article
- research article
- Published by S. Karger AG in Developmental Neuroscience
- Vol. 5 (2-3) , 243-251
- https://doi.org/10.1159/000112682
Abstract
The developmental pattern of the isoenzyme II of carbonic anhydrase (CAII; EC 4.2.1.1), a specific marker for oligodendroglia, was studied in the cerebella of thyroid-deficient, thyroxine-treated and undernourished rats, and compared with that in normal animals. In the normal cerebellum, the total CAII content was low during the first 10 postnatal days and increased maximally between 20 and 25 days. At first, all the CAII was present in the soluble fraction; the membrane-bound form was detected only from the age of about 13 days. At 40 days, the soluble and particulate forms represented about 70 and 30%, respectively, of the total CAII. The amount of CAII (expressed per cerebellum or per milligram of total soluble proteins) was markedly decreased in undernourishment and still more in thyroid deficiency. Thyroxine treatment induced a very precocious but only transient increase in the CAII content of the cerebellum. At the end of the experimental period studied (40 days), the CAII content was reduced to the same extent in the thyroxine-treated and undernourished rats. While undernutrition did not modify the percentage of soluble and membrane-bound CAII, thyroxine treatment and thyroid deficiency, respectively, accelerated and delayed the appearance of the particulate form. At the age of 35 days, the total number of oligodendrocytes in the white matter of cerebellum around the primary fissure remained unaffected in the thyroid-deficient rats, but it was reduced by 20 and 30% in the thyroxine-treated and undernourished animals, respectively; the effect of undernourishment was irreversible. These biochemical and histological results were discussed taking into consideration the differential effects of abnormal thyroid state and undernourishment on myelinogenesis.Keywords
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