Myelination and behaviour of tenascin-C null transgenic mice

Kiernan, B. W., Garcion, E., Ferguson, J., Frost, E. E., Torres, Eduardo Miguel, Dunnett, Stephen Bruce ORCID: https://orcid.org/0000-0003-1826-1578, Saga, Y., Aizawa, S., Faissner, A., Kaur, R., Franklin, R. J. M. and Ffrench-Constant, C. 1999. Myelination and behaviour of tenascin-C null transgenic mice. European Journal of Neuroscience 11 (9) , pp. 3082-3089. 10.1046/j.1460-9568.1999.00729.x

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Abstract

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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Publisher:	Wiley
ISSN:	0953-816X
Last Modified:	27 Oct 2022 09:37
URI:	https://orca.cardiff.ac.uk/id/eprint/66793

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