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Impaired sensory function in heterozygous P0 knockout mice is associated with nodal changes in sensory nerves
Author(s) -
Samsam M.,
Frei R.,
Marziniak M.,
Martini R.,
Sommer C.
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10115
Subject(s) - sensory system , knockout mouse , neuroscience , function (biology) , nodal , biology , anatomy , microbiology and biotechnology , genetics , gene
Mice heterozygously deficient in the major myelin component P0 are an established model of an inherited neuropathy and show signs of myelin degeneration in motor nerves. Unlike the case in patients, the sensory nerves are only mildly affected in the mouse mutants and do not show features indicative of myelin degeneration. Unexpectedly, by applying established behavioral tests, we found sensory deficits, as reflected by raised withdrawal thresholds to mechanical and thermal stimuli, whereas behavioral signs of a painful neuropathy were not detectable. By electron microscopy of longitudinal sections of sensory nerves, we found abnormalities in nodes of Ranvier comprising enlarged nodal gaps and poorly developed nodal Schwann cell microvilli. These alterations might be causally linked to the sensory deficits in the absence of profound myelin degeneration in the sensory nerves of the mutants. © 2002 Wiley‐Liss, Inc. © 2002 Wiley‐Liss, Inc.