RRC ID 46839
著者 Im SH, Takle K, Jo J, Babcock DT, Ma Z, Xiang Y, Galko MJ.
タイトル Tachykinin acts upstream of autocrine Hedgehog signaling during nociceptive sensitization in Drosophila.
ジャーナル Elife
Abstract 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.
巻・号 4
ページ e10735
公開日 2015-11-17
DOI 10.7554/eLife.10735
PII e10735
PMID 26575288
PMC PMC4739760
MeSH Action Potentials Animals Drosophila / physiology* Drosophila / radiation effects Drosophila Proteins / metabolism Electrophysiological Phenomena Hedgehog Proteins / metabolism* Hot Temperature Nociceptors / physiology* Receptors, Neurotransmitter / metabolism Signal Transduction* Tachykinins / metabolism*
IF 7.08
引用数 26
WOS 分野 BIOLOGY
リソース情報
ショウジョウバエ 8261R-1 4637R-2