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The Journal of Neuroscience, July 1, 2009, 29(26):8612-8619; doi:10.1523/JNEUROSCI.1057-09.2009

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Cellular/Molecular
Mrgprd Enhances Excitability in Specific Populations of Cutaneous Murine Polymodal Nociceptors

Kristofer K. Rau,¹ Sabrina L. McIlwrath,¹ Hong Wang,² Jeffrey J. Lawson,¹ Michael P. Jankowski,¹ Mark J. Zylka,² David J. Anderson,³ and H. Richard Koerber¹

¹Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, ²Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, and ³Division of Biology, Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125

Correspondence should be addressed to H. Richard Koerber, Department of Neurobiology, W1413 BSTWR, University of Pittsburgh, Pittsburgh, PA 15261. Email: rkoerber{at}pitt.edu

The Mas-related G protein-coupled receptor D (Mrgprd) is selectively expressed in nonpeptidergic nociceptors that innervate the outer layers of mammalian skin. The function of Mrgprd in nociceptive neurons and the physiologically relevant somatosensory stimuli that activate Mrgprd-expressing (Mrgprd⁺) neurons are currently unknown. To address these issues, we studied three Mrgprd knock-in mouse lines using an ex vivo somatosensory preparation to examine the role of the Mrgprd receptor and Mrgprd⁺ afferents in cutaneous somatosensation. In mouse hairy skin, Mrgprd, as marked by expression of green fluorescent protein reporters, was expressed predominantly in the population of nonpeptidergic, TRPV1-negative, C-polymodal nociceptors. In mice lacking Mrgprd, this population of nociceptors exhibited decreased sensitivity to cold, heat, and mechanical stimuli. Additionally, in vitro patch-clamp studies were performed on cultured dorsal root ganglion neurons from Mrgprd^–/– and Mrgprd^+/– mice. These studies revealed a higher rheobase in neurons from Mrgprd^–/– mice than from Mrgprd^+/– mice. Furthermore, the application of the Mrgprd ligand β-alanine significantly reduced the rheobase and increased the firing rate in neurons from Mrgprd^+/– mice but was without effect in neurons from Mrgprd^–/– mice. Our results demonstrate that Mrgprd influences the excitability of polymodal nonpeptidergic nociceptors to mechanical and thermal stimuli.

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Received March 4, 2009; revised April 28, 2009; accepted May 18, 2009.

Correspondence should be addressed to H. Richard Koerber, Department of Neurobiology, W1413 BSTWR, University of Pittsburgh, Pittsburgh, PA 15261. Email: rkoerber{at}pitt.edu

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