Myelin synthesis during postnatal nutritional deprivation and subsequent rehabilitation

Wiggins, R. C.; Miller, Sheldon L.; Benjamins, Joyce A.; Krigman, Martin R.; Morell, Pierre

doi:10.1016/0006-8993(76)90225-0

Cited by 117 publications

(55 citation statements)

References 25 publications

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“…Some data agree with a normal timing of myelinogenesis in undernourishment, i.e., only the quantity of myelin deposited might be reduced [17,19,23,39]. However, other workers have reported changes in the normal timing of deposition of the different myelin components, such as proteins [41] or gangliosides [43]. Because myelinogenesis is a very complex phenomenon, further investigations are necessary to understand better the mech anisms underlying the reduced myelination in the CNS of undernourished animals.…”

Section: Discussionsupporting

confidence: 49%

Effects of Abnormal Thyroid State and Undernutrition on Carbonic Anhydrase and Oligodendroglia Development in the Rat Cerebellum

Clos¹,

Legrand²,

Limozin

et al. 1982

Dev Neurosci

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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.

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Section: Discussionsupporting

confidence: 49%

Effects of Abnormal Thyroid State and Undernutrition on Carbonic Anhydrase and Oligodendroglia Development in the Rat Cerebellum

Clos¹,

Legrand²,

Limozin

et al. 1982

Dev Neurosci

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“…The high rate of oxidative metabolism is presumably associated with the enormous stress on the oligodendrocytes to maintain a membrane (myelin sheath), which can be 1OOx the weight of the cell (Morel1 and Toews, 1984). This high respiration rate and iron requirement is probably why oligodendrocytes are so highly vulnerable to conditions of metabolic stress such as cyanide toxicity (Bass, 1968) and postnatal starvation (Wiggins et al, 1976). Clearly the energy expenditure and hence iron requirement by oligodendrocytes for synthesis and maintenance of myelin is very high.…”

Section: Role Of Iron In Myelinationmentioning

confidence: 99%

Relationship of iron to oligondendrocytes and myelination

Connor

Menzies

1996

Glia

659

408

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“…Moreover, iron is thought to be involved in myelin production through its essential role in oxidative metabolism. A high rate of oxidative metabolism has been suggested to be associated with the unusual stress upon oligodendrocytes of metabolically maintaining membrane sheaths that can be one hundred times the weight of the cell body [Wiggins et al, 1974[Wiggins et al, , 1976.…”

Section: Introductionmentioning

confidence: 99%

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

Morath

Mayer-Pröschel

2002

Dev Neurosci

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One of the hallmarks of the pathology of iron deficiency in children is neurological disabilities that are often associated with hypomyelination. It has been hypothesized that this amyelination is mainly due to a disruption of myelin generation during the early postnatal stages when oligodendrocytes mature to generate myelin producing cell. In addition to these suggestions, we have previously provided in vitro data showing that iron affects both the proliferation and differentiation of glial precursor cells leading to a disruption in the generation of oligodendrocytes. We now present evidence demonstrating in vivo that iron deficiency during pregnancy affects the iron levels of various brain tissues in the developing fetus and disrupts not only the proliferation of their glial precursor cells but also disturbs the generation of oligodendrocytes from these precursor cells. In addition, we show that iron deficiency during embryogenesis affects glial lineage cells in a tissue-specific manner. Our studies offer the possibility to begin to comprehend whether any effects that occur during embryogenesis might have an influence on the establishment of the pathological defects that occur as a consequence of iron deficiency.

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Myelin synthesis during postnatal nutritional deprivation and subsequent rehabilitation

Cited by 117 publications

References 25 publications

Effects of Abnormal Thyroid State and Undernutrition on Carbonic Anhydrase and Oligodendroglia Development in the Rat Cerebellum

Effects of Abnormal Thyroid State and Undernutrition on Carbonic Anhydrase and Oligodendroglia Development in the Rat Cerebellum

Relationship of iron to oligondendrocytes and myelination

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

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