Department of Neurobiology; Yang Xiang Lab; Graduate School of Biomedical Sciences, Neuroscience Program
Molecular and Cellular Neuroscience
Pain signaling in vertebrates is modulated by neuropeptides like Substance P (SP). To determine whether such modulation is conserved and potentially uncover novel interactions between nociceptive signaling pathways we examined SP/Tachykinin signaling in a Drosophila model of tissue damage-induced nociceptive hypersensitivity. Tissue-specific knockdowns and genetic mutant analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are required for damage-induced thermal nociceptive sensitization. Electrophysiological recording showed that DTKR99D is required in nociceptive sensory neurons for temperature-dependent increases in firing frequency upon tissue damage. DTKR overexpression caused both behavioral and electrophysiological thermal nociceptive hypersensitivity. Hedgehog, another key regulator of nociceptive sensitization, was produced by nociceptive sensory neurons following tissue damage. Surprisingly, genetic epistasis analysis revealed that DTKR function was upstream of Hedgehog-dependent sensitization in nociceptive sensory neurons. Our results highlight a conserved role for Tachykinin signaling in regulating nociception and the power of Drosophila for genetic dissection of nociception.
Drosophila melanogaster, neuroscience
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© 2015, Im et al. This article is distributed under the terms of theCreative Commons Attribution Licensepermitting unrestricted use and redistribution provided that the original author and source are credited.
DOI of Published Version
Elife. 2015 Nov 17;4. pii: e10735. doi: 10.7554/eLife.10735. Link to article on publisher's site
Im, Seol Hee; Takle, Kendra; Jo, Juyeon; Babcock, Daniel T.; Ma, Zhiguo; Xiang, Yang; and Galko, Michael J., "Tachykinin acts upstream of autocrine Hedgehog signaling during nociceptive sensitization in Drosophila" (2015). Open Access Articles. 2664.
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This work is licensed under a Creative Commons Attribution 4.0 License.