Source:http://linkedlifedata.com/resource/pubmed/id/10510172
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
1999-11-24
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| pubmed:abstractText |
The extracellular matrix glycoprotein tenascin-C is widely expressed during development and repair, making it surprising that few abnormalities have been found in transgenic mice lacking this molecule. We have therefore re-examined the transgenic mice described by Saga et al. [Saga, Y., Yagi, T., Ikawa, Y., Sakakura, T. & Aizawa, S. (1992) Genes Dev., 6 1821-1831] in which tenascin-C was knocked-out by homologous recombination, focusing on two aspects of the nervous system likely to reveal any abnormalities that might follow the loss of tenascin-C. First, we have determined the pattern of myelin and distribution of oligodendrocyte precursor cells in those areas, such as the optic nerve and retina where local concentrations of tenascin-C have been proposed to act as barriers to oligodendrocyte precursor migration and so prevent inappropriate myelination. Secondly, we have examined the behaviour of the mice in a number of well-characterized tests, e.g. beam-walking, passive avoidance and the Morris water maze. We find no abnormalities of myelination or oligodendrocyte precursor distribution in adult mice, showing that local concentrations of tenascin-C are not the sole mechanism responsible for the pattern of myelination in these regions of CNS. However, we do find a number of behavioural abnormalities in these mice and show that hyperlocomotion and deficits in coordination during beam walking can be ascribed to tenascin-C deficiency. The effects on coordination are, however, not seen on a 129 genetic background. Taken together, these results significantly extend the phenotype associated with tenascin-C deficiency but argue against a role in myelination.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0953-816X
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| pubmed:author |
pubmed-author:AizawaSS,
pubmed-author:DunnettS BSB,
pubmed-author:FaissnerAA,
pubmed-author:FergusonJJ,
pubmed-author:FranklinR JRJ,
pubmed-author:FrostE EEE,
pubmed-author:GarcionEE,
pubmed-author:KaurRR,
pubmed-author:KiermanC CCC,
pubmed-author:SagiAA,
pubmed-author:TorresE MEM,
pubmed-author:ffrench-ConstantCC
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| pubmed:issnType |
Print
|
| pubmed:volume |
11
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3082-92
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| pubmed:dateRevised |
2009-9-29
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| pubmed:meshHeading |
pubmed-meshheading:10510172-Animals,
pubmed-meshheading:10510172-Avoidance Learning,
pubmed-meshheading:10510172-Behavior, Animal,
pubmed-meshheading:10510172-Exploratory Behavior,
pubmed-meshheading:10510172-Female,
pubmed-meshheading:10510172-Fluorescent Antibody Technique, Direct,
pubmed-meshheading:10510172-Heterozygote,
pubmed-meshheading:10510172-Immunohistochemistry,
pubmed-meshheading:10510172-In Situ Hybridization,
pubmed-meshheading:10510172-Male,
pubmed-meshheading:10510172-Maze Learning,
pubmed-meshheading:10510172-Mice,
pubmed-meshheading:10510172-Mice, Inbred C57BL,
pubmed-meshheading:10510172-Mice, Transgenic,
pubmed-meshheading:10510172-Motor Activity,
pubmed-meshheading:10510172-Myelin Basic Proteins,
pubmed-meshheading:10510172-Myelin Sheath,
pubmed-meshheading:10510172-Postural Balance,
pubmed-meshheading:10510172-Reflex,
pubmed-meshheading:10510172-Species Specificity,
pubmed-meshheading:10510172-Startle Reaction,
pubmed-meshheading:10510172-Tenascin
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| pubmed:year |
1999
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| pubmed:articleTitle |
Myelination and behaviour of tenascin-C null transgenic mice.
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| pubmed:affiliation |
Wellcome/CRC Institute of Developmental Biology and Cancer, Cambridge, UK.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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