Lipid Metabolism in Wallerian Degeneration

Domonkos, J

doi:10.1007/978-1-4615-7172-8_5

Cited by 10 publications

(3 citation statements)

References 66 publications

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“…The distal stump of a transected peripheral nerve undergoes Wallerian degeneration, a complex process involving dissolution of the axon and degradation of the myelin sheath (for reviews, see Rossiter, 196 1 ;Domonkos, 1972;Smith and Benjamins, 1984). The metabolic alterations reported with respect to lipid synthesis during Wallerian degeneration vary, depending on the precursor studied.…”

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Lipid Metabolism During Early Stages of Wallerian Degeneration in the Rat Sciatic Nerve

White

Toews

Goodrum

et al. 1989

Journal of Neurochemistry

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We examined changes in biosynthetic capacity of sciatic nerve during the early stages of Wallerian degeneration, utilizing a model that permits exclusion of nonresident cells from degenerating nerve. Sciatic nerve segments were placed in either 5-microns pore (allowing infiltration of nonresident cells) or 0.22-microns pore (excluding nonresident cells) Millipore diffusion chambers and then implanted in the peritoneal cavity of the same 32-34-day-old rat. At times up to 7 days postsurgery, nerve segments from the chambers, as well as control segments from the contralateral sciatic nerve, were removed and their capacity to incorporate radioactive precursors into lipids and proteins assayed in vitro. In nerve segments from both the 0.22- and 5-microns pore chambers, incorporation of [14C]acetate into total lipids was decreased relative to control by 50% at 12 h postsurgery and by 85% at day 3. This decreased incorporation of [14C]acetate reflects primarily decreased de novo synthesis of cholesterol and of fatty acyl residues incorporated into glycerolipids and sphingolipids. There was a preferentially decreased synthesis of cerebrosides and cholesterol (components enriched in myelin) relative to other lipids, while cholesterol esters and free fatty acids (products of membrane degradation) accounted for a greater proportion of the greatly reduced levels of total lipid label. In contrast to [14C]acetate, incorporation of [3H]glycerol into lipids was increased up to fourfold, relative to control, 1 day after nerve transection.(ABSTRACT TRUNCATED AT 250 WORDS)

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Lipid Metabolism During Early Stages of Wallerian Degeneration in the Rat Sciatic Nerve

White

Toews

Goodrum

et al. 1989

Journal of Neurochemistry

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“…Transection or crush of a peripheral nerve results in a characteristic and reproducible degeneration of the distal portion. This process, Wallerian degeneration, has been studied extensively as a model of demyelination secondary to axonal degeneration; the results of such investigations have been reviewed (Johnson e t al., 1949a;Rossiter, 1961;Domonkos, 1972;Smith and Benjamins, 1977). Dissolution of the axonal cytoskeleton, myelin ovoid formation, cellular proliferation and infiltration, transformation of myelin to sudanophilic lipid droplets, and axonal sprouting and remyelination occur sequentially.…”

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Early Stimulation of Phosphatidylcholine Biosynthesis During Wallerian Degeneration of Rat Sciatic Nerve

Natarajan

Yao

Dyck

et al. 1982

Journal of Neurochemistry

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Phospholipid metabolism was studied in rat sciatic nerve during Wallerian degeneration induced by crush injury. Portions of crushed sciatic nerve, incubated with labeled substrates, showed significantly higher phosphatidylcholine synthesis than normal nerve, prior to any measurable alterations of phospholipid composition. Maximum synthesis occurred 3 days after crush injury, at which time the metabolism of other phospholipids was unchanged. After a rapid decrease in biosynthetic activity, a second phase of enhanced phosphatidylcholine synthesis occurred, beginning 6 days after crush injury. Increased incorporation of [33P]phosphate, [2-3H]glycerol, and [Me-14C]choline indicated stimulation of de novo synthesis of phosphatidylcholine 3 days after injury. Neither base exchange reactions nor sequential methylation of ethanolamine phospholipids contributed significantly to phosphatidylcholine synthesis. Assay of certain key enzymes under optimal conditions in subcellular fractions of sciatic nerve revealed higher activities of cholinephosphate cytidyltransferase, choline phosphotransferase, and acyl-CoA:lysophosphatidylcholine acyltransferase in injured nerve, while choline kinase activity remained unchanged. This indicates that stimulation of phosphatidylcholine synthesis occurs via the cytidine nucleotide pathway, as well as by increased acylation of lysophosphatidylcholine. Although the cause of stimulated phosphatidylcholine synthesis remains unexplained, it is possible that trace amounts of lysophospholipids or other metabolites produced by injury-enhanced phospholipase activity may be responsible.

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“…This model also has the great advantage that the time sequence of myelin breakdown can be accurately followed. These extensive biochemical studies have been reviewed in detail Domonkos, 1972;Procellati, 1972) and are also described in Chapter 13.…”

Section: W Allerian Degenerationmentioning

confidence: 99%

Myelin

1977

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Lipid Metabolism in Wallerian Degeneration

Cited by 10 publications

References 66 publications

Lipid Metabolism During Early Stages of Wallerian Degeneration in the Rat Sciatic Nerve

Lipid Metabolism During Early Stages of Wallerian Degeneration in the Rat Sciatic Nerve

Early Stimulation of Phosphatidylcholine Biosynthesis During Wallerian Degeneration of Rat Sciatic Nerve

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