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L H Adcock

Publications and source records attributed to L H Adcock.

8 recordsLinked to original sources
PubMed1983

Hypomyelinated mutant mice. V. Relationship between jp and jpmsd re-examined on identical genetic backgrounds.

jp and jpmsd, two allelic mutations in the mouse that sharply reduce the amount of CNS myelin, produce diseases that can be distinguished morphologically only by their severity. This has raised the question of whether the two mutations are truly distinguishable. Since the two mutations have never been maintained on the same genetic background, correct quantitative and morphological comparison have not been possible. We have prepared a B6C3H stock of jp on the same genetic background as the available stock of jpmsd. In this jp stock, behavioral abnormalities, relative proportion of myelinated axons, and major morphological characteristics of the disease in situ are unchanged from the previous jp stock. The jp disease continues to be more severe than that of jpmsd. However, tissue from the new B6C3H stock myelinates better in organotypic culture than previous jp stocks. The increase in myelination is advantageous, not only for accurate comparison of the two alleles but for all culture studies of jp. Strictly comparable strains or stocks should be utilized in any comparative studies of closely related mutations such as jp and jpmsd.

Alleles↗
PubMed1983

Myelination of jp,jpmsd, and qk axons by normal glia in vitro: ultrastructural and autoradiographic evidence.

Normal optic nerve glia were 'injected' into hypomyelinated mutant jp,jpmsd, and qk cerebellum by co-culturing explants in direct physical contact. Quantitative light microscopic studies demonstrated that such glial injection significantly increased the number of myelin profiles counted in cultures, suggesting that axons in all 3 mutants can accept myelination from competent glia when they are made available. In each mutant, the observed increase in myelination was independent of the ages of donor optic nerves and recipient cultures, but absolutely required positioning of the optic nerve so that direct contact occurred with the mutant cerebellar explants. The additional myelin found near the zone of fusion with the optic nerve morphologically resembled normal, not mutant myelin. Autoradiographs made after [3H]thymidine-labeled normal optic nerve was injected into jpmsd cultures showed that labeled cells had colonized the nearby mutant tissue. Labeled cells identified as oligodendrocytes by ultrastructural criteria were found adjacent to myelin segments near the fusion zone, but direct continuity between processes of these oligodendrocytes and myelin sheaths was not demonstrated. The astrocytes and phagocytic cells which were also labeled had no obvious relationship to myelinated axons. These results provide experimental evidence that the primary abnormalities produced by the three mutations jp,jpmsd, and qk are inherent in their glial cells, probably although not definitely in the oligodendrocytes.

Animals↗
PubMed1981

Hypomyelinated mutant mice IV: peripheral myelin in jp msd.

This study compares peripheral myelination in a specific subdivision of the sciatic nerve of jp msd and unaffected littermate mice. No significant differences are found in numbers of myelinated and unmyelinated axons, diameters of axons, thickness of myelin sheaths relative to axon diameter, extent of unmyelinated axons segregation by Schwann cell processes, or in the ultrastructure of myelin and Schwann cells. By contrast, jp msd mutant mice show severe CNS hypomyelination. This evidence, that the jp msd mutation affects only oligodendrocytes, distinguishes mutations at this locus from others producing CNS hypomyelination in which PNS myelin is also affected.

Animals↗
PubMed1980

Hypomyelinated mutant mice. II. Myelination in vitro.

Organotypic cultures of cerebellum from hypomyelinated mutant mice provide a powerful experimental system for studying the cell biology of the mutant diseases. We have examined the extent to which the culture system reproduces the diseases of three well-known mutants, qk, jpmsd, and jp. Quantitation of myelin profiles per sq. mm of section demonstrates that in vitro, as in situ, qk produces the most myelin jpmsd an intermediate amount, and jp the least. Myelin in qk cultures is unique in being invisible by light microscopy of the living culture. Hypomyelination of jp may be more severe in vitro than in situ. Cultures of jpmsd exhibit many of the ultrastructural features of cerebellar abnormalities that occur in situ: degree of hypomyelination, clustering of myelin segments, scarcity of oligodendrocytes, absence of nodes of Ranvier but presence of heminodes, and apparent structural integrity of the myelin sheaths. Correspondence between in vitro and in situ ultrastructure is more difficult to assess for jp, because the available sample of jp myelin in vitro is too small, and for qk, because the abnormalities observed in situ resemble nonspecific abnormalities of normal myelin in vitro.

Animals↗
PubMed1980

Hypomyelinated mutant mice: description of jpmsd and comparison with jp and qk on their present genetic backgrounds.

Hypomyelinated mutant mice are valuable natural animal systems for analysis of CNS myelin development, chemistry and diseases. One mutant, jpmsd, has never received thorough morphological description. We here describe the detailed morphology of jpmsd, compare it with well-studied jp and qk on their present genetic backgrounds, and discuss the genetic histories of all 3 mutants. Region for region, jpmsd has twice as much myelin as jp, but 1/2--1/5 as much as qk. Both jp and jpmsd have scarce oligodendrocytes, rare nodes of Ranvier, clustering of myelin segments, abnormal lipid-filled cells, frequent degenerating cells, and rare distorted myelin profiles. In contrast, qk has abnormally numerous oligodendrocytes, frequent nodes of Ranvier, no obvious myelin clustering, no lipid-filled cells, rare degenerating cells, and frequent abnormal or distorted myelin profiles. jp and jpmsd are quantitatively different, but qualitatively similar. Since its origin, the jpmsd disease has inadvertently been ameliorated by transferring the mutation to a different background. Persistent differences in the remainder of the genome might account for all remaining apparent differences between jp and jpmsd. In contrast, qk is totally dissimilar in morphology and presumably in pathophysiology.

Animals↗