Adrenalectomy of Rats Results in Hypomyelination of the Central Nervous System

Abstract

The effect of adrenalectomy on CNS myelin accumulation was investigated to determine whether glucocorticoids play a role in regulating myelination. When 14-day-old rats were adrenalectomized and sacrificed 7-8 days later, the amount of bulk-isolated myelin in whole brain, as expressed per gram wet weight of brain or per milligram DNA-phosphate, was reduced to about 75% that of sham-operated controls. Both brain weight and DNA content were unchanged by adrenalectomy. Examination of individual brain regions also revealed decreased amounts of myelin in adrenalectomized animals. Brain glycerol 3-phosphate dehydrogenase specific activity was reduced in adrenalectomized animals to 40-60% that of controls, and serum corticosterone levels were less than 0.6% of control levels. The amount of cerebral myelin in animals adrenalectomized on day 21 and sacrificed 9 days later was not significantly reduced. This suggests a possible role of glucocorticoids during the early period of rapid myelination.

Dexamethasone Stimulates the Biochemical Differentiation of Fetal Forebrain Cells in Reaggregating Cultures

“…All these studies were carried out on intact animals given large doses of exoge nous hormone. Recently, it was shown that if adrenalectomy is carried out at approxi mately the same age as in our study (11-14-day-old rats), bulk-isolated myelin from whole brain was reduced to about 75% shortly after adrenalectomy, but brain weight, DNA content and CNP activity were not modified [Preston and McMorris, 1984], In contrast, increases in myelin deposition, brain weight, DNA, and protein content as well as CNP activity were observed 7-8 weeks after adrenalectomy [Meyer, 1983]. This author reports that the changes caused by the removal of the adrenals can be at least partially reversed by chronic glucocorticoid replacement therapy [Meyer, 1983].…”

“…Myelination of the brain has been re ported to be accelerated [Casper et al, 1967;Preston and McMorris, 1984], or retarded by administration of corticosteroids [Howard and Benjamins, 1975;Noguchi et ah, 1982;Bohn and Friedrich, 1982;Meyer, 1983]. Bohn and Friedrich [1982] showed that the reduction in myelin formation and deposition in the optic nerve of the rat caused by cortisol treatment was fully recovered 6 weeks after cessation of the drug.…”

Intrinsic expression of transcortin in neural cells of the mouse brain: a histochemical and molecular study

“…A portion of the oligodendrocytes also contained CBG, as shown by double immunostaining with CNPase. The complex role of GCs in the maturation of oligodendrocytes and myelinogenesis has been demonstrated (Preston and McMorris, 1984;Raschke et al, 2008) and could be explained by documented expression of GC receptors in oligodendrocyte progenitor cells (Bohn et al, 1991). Currently, high doses of GCs are widely used in the treatment of multiple sclerosis, a well-described disease characterized by oligodendrocyte degeneration.…”

Oligodendrocytes as glucocorticoids target cells: functional analysis of the glycerol phosphate dehydrogenase gene

“…The significance of the glucocorticoid regulation of GPDH to oligodendrocyte function needs to be further investigated because glucocorticoids enhance oligodendrocyte differentiation and myelination in vivo (Preston and McMorris, 1984) and in vitro (Kumar et al, 1989;Warringa et al, 1987;Lopez-Cardozo et al, 1989;Byravan and Campagnoni 1994;Chan et al, 1998). For instance, glucocorticoids increase proteolipid protein and myelin basic protein mRNAs in oligodendrocytes by a posttranscriptional mechanism (Kumar et al, 1989).…”