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1 Neuroscience, Max-Delbruck Center for Molecular Medicine, Berlin, Berlin, Germany
2 Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
3 Life Sciences Division,, Lawrence Berkeley National Laboratory, University of California, Berkeley, Berlin, Germany
4 New York Blood Center, United States
* To whom correspondence should be addressed. E-mail: glewin{at}mdc-berlin.de.
Somatic sensory neurons of the dorsal root ganglia are necessary for a large part of our mechanosensory experience. However, we only have a good knowledge of the molecules required for mechanotransduction in simple invertebrates such as the nematode Caenorhabiditis elegans. In C.elegans a number of so-called mec genes have been isolated that are required for the transduction of body touch. One such gene, mec-2 codes for an integral membrane protein of the stomatin family, a large group of genes with a stomatin homology domain. Using stomatin null mutant mice we have tested the hypothesis that the founding member of this family, stomatin might play a role in the transduction of mechanical stimuli by primary sensory neurons. We used the in vitro mouse skin nerve preparation to record from a large population of low threshold and high threshold mechanoreceptors with myelinated A-fiber (n=553) and unmyelinated C-fiber (n=157) axons. One sub-type of mechanoreceptor, the D-hair receptor which is a rapidly adapting mechanoreceptor, had reduced sensitivity to mechanical stimulation in the absence of stomatin. Other cutaneous mechanoreceptors, including nociceptive C-fibers were not affected by the absence of a functional stomatin protein. Patch clamp analysis of presumptive D-hair mechanoreceptive neurons, which were identified by a characteristic rosette morphology in culture, showed no change in membrane excitability in the absence of the stomatin protein. We conclude that stomatin is required for normal mechanotransduction in a sub-population of vertebrate sensory neurons.
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