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At least 469 records · Page 26Linked to original sources
PubMed1999

Quaking*shiverer double-mutant mice survive for at least 100 days with no CNS myelin.

Mice expressing mutations that produce CNS hypomyelination often die prematurely: the more severe the hypomyelination, the shorter the life span. However, we have previously described jimpy-msd mice that survive twice as long as usual; although they acquire significantly increased amounts of myelin, they still succumb long before their unaffected littermates. This result contradicts any postulated causal relationship between extent of CNS hypomyelination and premature death of the animal. Here we have addressed this question in another way, by using an animal model that does not involve a proteolipid protein (Plp) gene mutation. We demonstrate that quaking*shiverer double-mutant mice can survive for at least 100 days without any CNS myelin whatsoever. Therefore, at least for a mouse, absence of CNS myelin is not lethal per se.

Animals↗
PubMed1995

Conditionally immortalized oligodendrocyte cell lines migrate to different brain regions and elaborate 'myelin-like' membranes after transplantation into neonatal shiverer mouse brains.

Five immortalized oligodendrocyte cell lines, representing a spectrum of different stages of oligodendrocyte maturation, were transplanted into neonatal shiverer mouse brains and examined for their ability to survive, multiply, and migrate in vivo. Each of the cell lines migrated to different regions of the brain with remarkable consistency when injected into the mouse forebrain, suggesting that the cells might be responding to different environmental cues present in the neonatal mouse brain. These results are consistent with the fact that cells at different stages in the oligodendrocyte lineage probably possess different sets of surface molecules and receptors. Significant differences were also observed in the survival and proliferation of the lines examined, even when the lines tested had quite similar in vitro phenotypes. Interestingly, the cell line with the most mature in vitro phenotype, N20.1, appeared to elaborate membranous processes when transplanted into the brain, reminiscent of oligodendrocytes ensheathing axonal segments. The experiments suggest that these immortalized cells could be useful models to study the cellular and molecular mechanisms involved in the development, maturation and possibly formation of myelin by oligodendrocytes in the mammalian brain.

Animals↗
PubMed1993

Generation and analysis of normal and shiverer temperature-sensitive immortalized cell lines exhibiting phenotypic characteristics of oligodendrocytes at several stages of differentiation.

Normal glial cells immortalized at specific developmental stages would be useful tools with which to study glial cell differentiation in vitro. Similarly, immortalized glial cell lines derived from known neurological mutants with identified developmental, molecular genetic defects would also be useful for the in vitro examination of the effects of the mutation on glial cell function. In this report we describe the immortalization of 19 separate oligodendroglial cell lines, 10 derived from normal mice and 9 derived from the neurological mutant shiverer, which is missing a large segment of the myelin basic protein gene. Enriched oligodendrocyte cultures prepared at 7 days in vitro, a time when the majority of the cells were oligodendrocyte precursors undergoing transition into mature oligodendrocytes, were immortalized with pZIPSVtsA58, which carries a temperature-sensitive immortalizing oncogene. All of the immortalized cell lines grew rapidly at the permissive temperature of 34 degrees C and exhibited a dramatic decrease in growth rate at the nonpermissive temperature of 39 degrees C. The cell lines were characterized by immunocytochemistry and Northern blot analysis for a number of glial cell markers, and the phenotype of all the lines were consistent with their being in the oligodendroglial cell lineage. The phenotypes of the cell lines varied significantly with representatives of oligodendrocyte precursors, and immature and mature oligodendrocytes being present within the population of immortalized lines. All the cell lines appeared to be clonal based upon Southern blot analysis and all have been passaged at least 40 times with retention of stable phenotype.

Animals↗
PubMed1990

Normal composition of the major lipids and the distribution of their fatty acids in central nervous system myelin further discriminate mld from shiverer mice.

The primary defect in myelin deficiency (mld), an autosomal recessive mutation in mice with severe hypomyelination of the central nervous system (CNS), is a reduction in the synthesis of myelin basic protein (MBP) due to reduced amounts of MBP-specific mRNA. The present study was performed to determine whether alterations of myelin lipid composition might be associated with this defect. Although a 20-fold reduction of myelin was found in mld brain, the lipid/protein and the phospholipid/sulfatide ratios of purified myelin were unchanged. The analysis of polar lipids demonstrated no striking difference. However, phosphatidylethanolamine (including plasmalogens of the ethanolamine type) was decreased by 7.7% in mld. Fatty acids of total and polar lipids (phospholipids + glycolipids) exhibited a slight decrease in 20:1(n-11) and 20:1(n-9). In conclusion, these results further differentiate mld from its allele shiverer, which shares with mld a dramatic reduction of MBP and absence of major dense line but, in contrast, presents other important biochemical differences in CNS myelin.

Animals↗
PubMed1990

Transfection of transformed shiverer mouse glial cell lines.

In the course of studies on glial cell differentiation in the mouse mutant shiverer, we have established by infection with a temperature-sensitive retrovirus encoding the SV40 T antigen a few glial cell lines that divide rapidly at 33 degrees C, the permissive temperature, and whose phenotypes at the nonpermissive temperature (39 degrees C) resemble either astrocytes or oligodendrocytes. One astrocyte-like clone (clone SF11) expresses glial fibrillary acidic protein at 33 degrees C and expresses this marker strongly at 39 degrees C as well. One oligodendrocyte-like clone (DM5) that we have succeeded in maintaining at 33 degrees C can be induced to express galactocerebroside and 2',3'-cyclic nucleotide 3'-phosphodiesterase at the elevated temperature but never expresses the more differentiated markers of the myelination state, such as the myelin proteolipid protein or the myelin-associated glycoprotein. Clone DM5, as is the case with other oligodendrocyte clones we have prepared by the method described here, is quite fragile and survives for only several (5-6) days at the higher temperature. Both clonal lines can serve as host cells for expressible cDNAs introduced by transfection, such as the neurofilament protein, NF-M, and the small myelin basic protein.

Animals↗
PubMed1990

Non-shivering thermogenesis and brown adipose tissue activity in essential fatty acid deficient rats.

The effects of essential fatty acid (EFA) deficiency on energetic metabolism and interscapular brown adipose tissue (BAT) activity were examined in the cold acclimated rat. Weanling male Long-Evans rats were fed on a low fat semipurified diet (control diet, 2% sunflower oil; EFA deficient diet, 2% hydrogenated coconut oil) for 9 weeks. They were exposed at 5 degrees C for the last 5 weeks. In EFA deficient rats, compared to controls, growth retardation reached 22% at sacrifice. Caloric intake being the same in the two groups, it follows that food efficiency was decreased by 40%. Resting metabolism in relation to body surface area was 25% increased. Calorigenic effect of norepinephrine (NE) in vivo (test of non-shivering thermogenesis) underwent a marked decrease of 34%. BAT weight was 21% decreased but total and mitochondrial protein content showed no variation. A 26% increase in purine nucleotide binding per BAT (taken as an index of thermogenic activity) was observed, suggesting that the enhancement in resting metabolism observed was mainly due to increased BAT thermogenesis. However, BAT mitochondria respiratory studies which are more direct functional tests showed a marked impairment of maximal O2 consumption of about 30% with palmitoyl-carnitine or acetyl-carnitine (both in presence of malate) or with alpha-glycerophosphate as substrate. It is likely that this impaired maximal BAT oxidative capacity may explain the impaired NE calorigenic effect in vivo. A possible increase in mitochondrial basal permeability is also discussed.

Acclimatization↗