1. Metabolism of [(35)S]sulpholipid was studied in rats of different ages after the injection of [(35)S]sulphate. 2. The turnover of sulphatide in brain myelin and subcellular fractions was followed for long periods. 3. A small fraction of adult myelin underwent rapid metabolism, the rest being relatively metabolically stable. 4. Fast turnover of brain microsomal sulphatide during development was related to the process of myelination. 5. Turnover of mitochondrial sulphatide was at a lower rate than that calculated for liver mitochondria. 6. The relevance of the results to the metabolism of the whole membrane is discussed.

Animals↗

PubMed1966

Turnover of brain mitochondrial membrane lipids.

1. The turnover of lipids, of myelin and other brain subcellular particles has been studied in double-labelling experiments on intact rats. 2. Overall metabolism of brain mitochondrial lipids was three times slower than that of the liver. 3. Individual lipids of brain mitochondria and myelin were also separated and their metabolism was studied. 4. All myelin lipids examined undergo very slow turnover. Two pools of brain mitochondrial lipid were identified. The slowly metabolized lipids were cholesterol, cardiolipin plus phosphatidic acid and possibly sphingomyelin; the remaining phosphatides underwent more rapid turnover. 5. The possible significance of these results is discussed.

Journal Article↗

PubMed1965

The chemical composition of vertebrate myelin and microsomes.

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Animals↗

PubMedDate not supplied

The effect of 5-bromodeoxyuridine on remyelination in the peripheral nervous system of the mouse.

The thymidine analogue, 5-bromodeoxyuridine (BrdU), has been used in an attempt to manipulate experimentally the proliferative response of the Schwann cell population that follows induction of segmental demyelination in the peripheral nervous system. It was found that in the presence of BrdU, a significant number of Schwann cells displayed a susceptibility to the agent, in that they could be 'held' in the pro-myelinated state. It is suggested that there is some regulatory transition requiring the priming of the Schwann cell genome for myelination that occurs before the remyelinating phase of repair can be started, but after the establishment of the Schwann cell/axon relationship.

Animals↗