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J Neurophysiol 98: 3802-3808, 2007. First published October 17, 2007; doi:10.1152/jn.00860.2007
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Stomatin and Sensory Neuron Mechanotransduction

Carlos Martinez-Salgado*, Anne G. Benckendorff*, Li-Yang Chiang, Rui Wang, Nevena Milenkovic, Christiane Wetzel, Jing Hu, Cheryl L. Stucky, Marilyn G. Parra, Narla Mohandas and Gary R. Lewin

Department of Neuroscience, Max-Delbrück Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Berlin-Buch Germany

Submitted 2 August 2007; accepted in final form 17 October 2007

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- and high-threshold mechanoreceptors with myelinated A-fiber (n = 553) and unmyelinated C-fiber (n = 157) axons. One subtype 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 receptor 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 subpopulation of vertebrate sensory neurons.


Address for reprint requests and other correspondence: G. R. Lewin, Dept. of Neuroscience, Max-Delbrück Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Robert-Rössle Str., Berlin-Buch, D-13092, Germany (E-mail: glewin{at}mdc-berlin.de)




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