The lipids of white matter and peripheral nerve from mutant mice with known myelin deficiencies were analyzed by one- and two-dimensional high-performance thin-layer chromatography and quantitated by densitometry. In optic nerve, the mutants jp/Y, jpmsd/Y, qk/qk, shi/shi and shimld/shimld, which have severe central nervous system (CNS) myelin deficiency, had a common pattern of lipid loss: cerebrosides and sulfatides (hydroxy and nonhydroxy forms) were generally reduced by 70–95% or more; most phospholipids were diminished by 15–55%, and cholesterol was reduced by 35–60%. Only in the CNS of jp/Y and jpmsd/Y did cholesterol ester accumulate. In peripheral nerve, the lipid composition varied markedly among these mutants. In jp/Y there was no change, while in jpmsd/Y there was a 5–15% loss among the phospholipids and cholesterol. Homozygous qk had reductions of 75–85% in the nonhydroxy forms of cerebroside and sulfatide, a 130% increase in hydroxy sulfatide, and a 55% loss of sphingomyelin. In shi/shi and shimld/shimld homozygotes, the glycolipids were altered by ± 20%, most phospholipids and cholesterol were reduced by 5–15%, and sphingomyelin was reduced by 40%. Tr and TrJ showed 35–90% reductions in most lipid classes of the peripheral nervous system; CNS lipid composition was normal. Homozygous twi had a uniform loss of most lipid classes in both optic (generally 10–20%) and trigeminal nerves (generally 40–55%); cerebrosides did not accumulate in these tissues, dy/dy had a 10–20% reduction of cerebrosides in trigeminal nerve trunk. The CNS of dy homozygotes had 10–35% increases in specific classes of glycolipids and phospholipids, and in cholesterol. None of the mutants showed detectable levels of lysophospholipids or other unusual lipid species. The fractions of ethanolamine and choline phosphatides in the plasmalogen form were close to normal in all mutants.
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 axJ/axJ, there were increases of 20–30% in the levels of the major phospholipids; peripheral nerve was normal. In bc3J/bc3JCNS, 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 dtJ/dtJ, vb/vb and wr/wr, almost all lipids were significantly decreased. The CNS of dtJ/dtJand 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.
The lipids of white matter and peripheral nerve from mutant mice with known myelin deficiencies were analyzed by one- and two-dimensional high-performance thin-layer chromatography and quantitated by densitometry. In optic nerve, the mutants jp/Y, jpmsd/Y, qk/qk, shi/shi and shimld/shimld, which have severe central nervous system (CNS) myelin deficiency, had a common pattern of lipid loss: cerebrosides and sulfatides (hydroxy and nonhydroxy forms) were generally reduced by 70–95% or more; most phospholipids were diminished by 15–55%, and cholesterol was reduced by 35–60%. Only in the CNS of jp/Y and jpmsd/Y did cholesterol ester accumulate. In peripheral nerve, the lipid composition varied markedly among these mutants. In jp/Y there was no change, while in jpmsd/Y there was a 5–15% loss among the phospholipids and cholesterol. Homozygous qk had reductions of 75–85% in the nonhydroxy forms of cerebroside and sulfatide, a 130% increase in hydroxy sulfatide, and a 55% loss of sphingomyelin. In shi/shi and shimld/shimld homozygotes, the glycolipids were altered by ± 20%, most phospholipids and cholesterol were reduced by 5–15%, and sphingomyelin was reduced by 40%. Tr and TrJ showed 35–90% reductions in most lipid classes of the peripheral nervous system; CNS lipid composition was normal. Homozygous twi had a uniform loss of most lipid classes in both optic (generally 10–20%) and trigeminal nerves (generally 40–55%); cerebrosides did not accumulate in these tissues, dy/dy had a 10–20% reduction of cerebrosides in trigeminal nerve trunk. The CNS of dy homozygotes had 10–35% increases in specific classes of glycolipids and phospholipids, and in cholesterol. None of the mutants showed detectable levels of lysophospholipids or other unusual lipid species. The fractions of ethanolamine and choline phosphatides in the plasmalogen form were close to normal in all mutants.
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