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J Physiol Volume 545, Number 1, 43-50, November 15, 2002 DOI: 10.1113/jphysiol.2002.027656
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Journal of Physiology (2002), 545.1, pp. 43-50
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.027656

GFR alpha2/neurturin signalling regulates noxious heat transduction in isolectin B4-binding mouse sensory neurons

Cheryl L. Stucky*†, Jari Rossi‡, Matti S. Airaksinen‡ and Gary R. Lewin*

*Growth Factors and Regeneration Group, Department of Neuroscience, Max Delbrück Center for Molecular Medicine, Robert Rössle Str. 10, Berlin D-13092, Germany, ‡Program in Molecular Neurobiology, Institute of Biotechnology, Viikki Biocenter, 00014 University of Helsinki, Finland and †Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226-0509, USA

The GFR alpha2 receptor is the cognate co-receptor for the neurotrophic factor neurturin and GFR alpha2 is selectively expressed by isolectin B4 (IB4)-binding nociceptive sensory neurons. Here, we used two physiological approaches in combination with mice that have a targeted deletion of the GFR alpha2 gene (GFR alpha2 -/- mice) in order to determine whether GFR alpha2/neurturin signalling regulates the functional properties or the survival of IB4-binding nociceptors. Because 50 % of IB4-binding neurons respond to noxious heat and because patch clamp recordings of isolated dorsal root ganglion sensory neurons allow one to neurochemically identify subpopulations of neurons, we analysed the noxious heat responsiveness of IB4-positive and -negative small-diameter neurons isolated from adult GFR alpha2 -/- and littermate control mice. The percentage of IB4-positive neurons that had large (> 100 pA) heat-evoked inward currents was severely reduced in GFR alpha2 -/- mice (12 %) compared to wild-type littermates (47 %), and this loss in large-magnitude heat currents was accounted for by an increase in neurons with very small (< 100 pA) heat-evoked currents as well as an increase in neurons with no detectable heat current. Counts of IB4-positive and -negative neurons, as well as counts of unmyelinated axons in the saphenous nerve, confirmed that the loss in neurons with large-amplitude heat currents was due to a deficit in heat transduction and not a decrease in cell survival. The effect was modality specific for heat because mechanical transduction of all fibre types, including IB4-positive C fibres, was normal. Our data are the first to indicate a transduction-function role for GFR alpha2/neurturin signalling in a specific class of sensory neurons.



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