西亞試劑：Construction of a Global Pain Systems Network Highlights Ph

Construction of a Global Pain Systems Network Highlights Phospholipid Signaling as a Regulator of Heat Nociception

G. Gregory Neely1,2#*, Shuan Rao3#, Michael Costigan4#, Norbert Mair5, Ildiko Racz6, Giedre Milinkeviciute1, Arabella Meixner3, Swetha Nayanala7, Robert S. Griffin8, Inna Belfer9, Feng Dai9,10, Shad Smith11, Luda Diatchenko11, Stefano Marengo12, Bernhard J. Haubner3, Maria Novatchkova3, Dustin Gibson11, William Maixner11, J. Andrew Pospisilik13, Emilio Hirsch12, Ian Q. Whishaw14, Andreas Zimmer6, Vaijayanti Gupta7, Junko Sasaki15, Yasunori Kanaho16, Takehiko Sasaki15,17, Michaela Kress5, Clifford J. Woolf4, Josef M. Penninger3

The ability to perceive noxious stimuli is critical for an animal's survival in the face of environmental danger, and thus pain perception is likely to be under stringent evolutionary pressure. Using a neuronal-specific RNAi knock-down strategy in adult Drosophila, we recently completed a genome-wide functional annotation of heat nociception that allowed us to identify α2δ3 as a novel pain gene. Here we report construction of an evolutionary-conserved, system-level, global molecular pain network map. Our systems map is markedly enriched for multiple genes associated with human pain and predicts a plethora of novel candidate pain pathways. One central node of this pain network is phospholipid signaling, which has been implicated before in pain processing. To further investigate the role of phospholipid signaling in mammalian heat pain perception, we analysed the phenotype of PIP5Kα and PI3Kγ mutant mice. Intriguingly, both of these mice exhibit pronounced hypersensitivity to noxious heat and capsaicin-induced pain, which directly mapped through PI3Kγ kinase-dead knock-in mice to PI3Kγ lipid kinase activity. Using single primary sensory neuron recording, PI3Kγ function was mechanistically linked to a negative regulation of TRPV1 channel transduction. Our data provide a systems map for heat nociception and reinforces the extraordinary conservation of molecular mechanisms of nociception across different species.

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