Lipid class and fatty acid composition of intact peripheral nerve and during wallerian degeneration

Berry, James F.; Cevallos, William; Wade, R. R.

doi:10.1007/bf02540090

Cited by 145 publications

(51 citation statements)

References 44 publications

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“…Numerous lipid droplets had already accumulated within Schwann cells and resident macrophages (Fig. 4 A); based on previous biochemical studies, these droplets probably are cholesteryl esters (36)(37)(38)(39).…”

Section: Resultsmentioning

confidence: 65%

A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

Boyles¹,

Zoellner²,

Anderson³

et al. 1989

J. Clin. Invest.

500

269

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Recent work has demonstrated that apo E secretion and accumulation increase in the regenerating peripheral nerve. The fact that apoE, in conjunction with apoA-I and LDL receptors, participates in a well-established lipid transfer system raised the possibility that apoE is also involved in lipid transport in the injured nerve. In the present study of the crushed rat sciatic nerve, a combination of techniques was used to trace the cellular associations of apoE, apoA-I, and the LDL receptor during nerve repair and to determine the distribution of lipid at each stage. After a crush injury, as axons died and Schwann cells reabsorbed myelin, resident and monocyte-derived macrophages produced large quantities of apoE distal to the injury site. As axons regenerated in the first week, their tips contained a high concentration of LDL receptors. After axon regeneration, apoE and apoA-I began to accumulate distal to the injury site and macrophages became increasingly cholesterol-loaded. As remyelination began in the second and third weeks after injury, Schwann cells exhausted their cholesterol stores, then displayed increased LDL receptors. Depletion of macrophage cholesterol stores followed over the next several weeks. During this stage of regeneration, apoE and apoA-I were present in the extracellular matrix as components of cholesterol-rich lipoproteins. Our results demonstrate that the regenerating peripheral nerve possesses the components of a cholesterol transfer mechanism, and the sequence of events suggests that this mechanism supplies the cholesterol required for rapid membrane biogenesis during axon regeneration and remyelination.

show abstract

Section: Resultsmentioning

confidence: 65%

A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

Boyles¹,

Zoellner²,

Anderson³

et al. 1989

J. Clin. Invest.

500

269

View full text Add to dashboard Cite

show abstract

“…Thus there is a dramatic increase in the local concentration of LPC in nerves undergoing myelin degeneration [33]. It is known that the demyelinating effect of LPC is due to the LPC molecule as such and not to metabolites [20].…”

Section: Discussionmentioning

confidence: 99%

Influence of Fatty Acid Content of Lysophosphatidyl Choline on Its Myelinotoxic Properties

Sedal

Jennings²,

Allt³

et al. 1992

Eur Neurol

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The efficacy of lysophosphatidyl choline (LPC) type I and type IV in producing demyelination was assessed in rat tibial and sural nerve. By light and electron microscopy, a greater myelinolytic activity was demonstrated with type I, and concomitantly electrophysiology showed a more severe conduction block. In teased nerve preparations and 1-um thin sections, demyelinated fibres were more frequent with LPC type I. At 1 h after injection, electron microscopy showed much more extensive myelin lysis in the form of fine vesicular debris. By 6 days, completely demyelinated fibres were much more common and associated Schwann cells contained either small quantities or no myelin debris. With type IV LPC, cytopathological changes were more extensive at 1 h. A minority of Schwann cells showed swollen hydropic cytoplasm and degradation of organelles. Axonal retraction from the myelin sheath occurred in occasional fibres, and in a few unmyelinated fibres axoplasm showed organelle depletion and increased granularity. By 6 days, Schwann cells still contained large quantities of gross myelin debris and had often retracted to expose extensive areas of axolemma. The findings suggest that the two types of LPC have different myelinolytic actions, which may be related to their different fatty acid content. A possible role for the two types of LPC in ‘bystander demyelination’ is considered.

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“…the accumulation of CE and lysophospholipids, products which accumu late dramatically, for instance, in Wallerian degeneration [3,52]. Although the lipid com position of dtJldtJ peripheral nerve is greatly altered, we did not detect CE or lysophos pholipids in either younger animals (P19), in which fiber degeneration is ongoing, or in older animals (P45), in which sensory fiber loss is already complete [13,26].…”

Section: Mutants With Major Lipid Abnormalitiesmentioning

confidence: 49%

A Survey of Neurological Mutant Mice

Ganser

Kerner²,

Brown³

et al. 1988

Dev Neurosci

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The lipids of white matter and peripheral nerve from neurological mutant mice with possible myelin abnormalities were analyzed by thin-layer chromatography and quantitated by densitometry. Eight mutants had major abnormalities in the central nervous system (CNS) and/or peripheral nervous system (PNS) tissues examined (optic nerve, and trigeminal and sciatic nerves). In the optic nerve of ax^J/ax^J, there were increases of 20–30% in the levels of the major phospholipids; peripheral nerve was normal. In bc^3J/bc^3JCNS, the major phospholipids and cholesterol were increased by 25–40%; the PNS was normal. In myd/myd CNS, there were increases of about 20% in the levels of both forms of cerebrosides and in the major phospholipids; in the PNS the lipids were normal, ot/ot CNS had 20–40% reductions of all the glycolipids and minor alterations in some of the phospholipids and cholesterol; the PNS had 20% losses of both forms of cerebrosides. In the PNS of ji/ji, there were decreases of 10–40% among the glycolipids and of 15–25% in three of the major phospholipids; the CNS was virtually normal. In the PNS of dt^J/dt^J, vb/vb and wr/wr, almost all lipids were significantly decreased. The CNS of dt^J/dt^Jand vb/vb were normal; wr/wr had minor reductions of certain glycolipids and phospholipids. Six mutants had relatively minor lipid abnormalities in their myelinated tissues. In cr/cr PNS, there were elevated levels of the cerebrosides and major phospholipids; the CNS was virtually normal. In db/db CNS and PNS, there were reduced levels of the nonhydroxy forms of cerebroside and sulfatide. The major change in htr/htr was the elevation of all the glycolipids in the CNS. In the CNS of Lc/+, nonhydroxy cerebroside was reduced. In shm/shm PNS, nonhydroxy sulfatide was elevated and there were small decreases in some of the phospholipids, wl/wl CNS showed decreases among most of the glycolipids. Mutants homozygous for du, mto, spa and tg had virtually normal lipid levels in both the optic and peripheral nerves.

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Lipid class and fatty acid composition of intact peripheral nerve and during wallerian degeneration

Cited by 145 publications

References 44 publications

A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

Influence of Fatty Acid Content of Lysophosphatidyl Choline on Its Myelinotoxic Properties

A Survey of Neurological Mutant Mice

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