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Development of early postnatal peripheral nerve abnormalities in Trembler‐J and PMP22 transgenic mice by A. M. ROBERTSON; C. HUXLEY; R. H. M. KING; P. K. THOMAS is a scholarly article available to read on EtoBox.

What is Development of early postnatal peripheral nerve abnormalities in Trembler‐J and PMP22 transgenic mice about?

Mutations in the gene for peripheral myelin protein 22 (__PMP22__) are associated with peripheral neuropathy in mice and humans. Although PMP22 is strongly expressed in peripheral nerves and is localised largely to the myelin sheath, a dual role has been suggested as 2 differentially expressed promoters have been found. In this study we compared the initial stages of postnatal development in transgenic mouse models which have, in addition to the murine __pmp22__ gene, 7 (C22) and 4 (C61) copies of the human __PMP22__ gene and in homozygous and heterozygous Trembler‐J (__Tr__^__J__^) mice, which have a point mutation in the __pmp22__ gene. The number of axons that were singly ensheathed by Schwann cells was the same in all groups indicating that PMP22 does not function in the initial ensheathment and separation of axons. At both P4 and P12 all mutants had an increased proportion of fibres that were incompletely surrounded by Schwann cell cytoplasm indicating that this step is disrupted in PMP22 mutants. C22 and homozygous __Tr__^__J__^ animals could be distinguished by differences in the Schwann cell morphology at the initiation of myelination. In homozygous __Tr__^__J__^ animals th

Author

A. M. ROBERTSON; C. HUXLEY; R. H. M. KING; P. K. THOMAS

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0021-8782)

Published

1999

Language

EN