• Sarah E Ross, Alan R Mardinly, Alejandra E McCord, Jonathan Zurawski, Sonia Cohen, Cynthia Jung, Linda Hu, Stephanie I Mok, Anar Shah, Erin M Savner, Christos Tolias, Roman Corfas, Suzhen Chen, Perrine Inquimbert, Yi Xu, Roderick R McInnes, Frank L Rice, Gabriel Corfas, Qiufu Ma, Clifford J Woolf, and Michael E Greenberg.
• Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
• Neuron. 2010 Mar 25; 65 (6): 886-98.

AbstractItch is the least well understood of all the somatic senses, and the neural circuits that underlie this sensation are poorly defined. Here we show that the atonal-related transcription factor Bhlhb5 is transiently expressed in the dorsal horn of the developing spinal cord and appears to play a role in the formation and regulation of pruritic (itch) circuits. Mice lacking Bhlhb5 develop self-inflicted skin lesions and show significantly enhanced scratching responses to pruritic agents. Through genetic fate-mapping and conditional ablation, we provide evidence that the pruritic phenotype in Bhlhb5 mutants is due to selective loss of a subset of inhibitory interneurons in the dorsal horn. Our findings suggest that Bhlhb5 is required for the survival of a specific population of inhibitory interneurons that regulate pruritus, and provide evidence that the loss of inhibitory synaptic input results in abnormal itch.(c) 2010 Elsevier Inc. All rights reserved.

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