Journal
CURRENT BIOLOGY
Volume 26, Issue 23, Pages 3116-3128Publisher
CELL PRESS
DOI: 10.1016/j.cub.2016.09.038
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Funding
- NIH National Institute of Child Health and Human Development Training Grant [NIH T32-HD07325]
- NIH Predoctoral Kirschstein National Research Service Award (NRSA) Fellowship (National Institute of Neurological Disorders and Stroke [NINDS]) [F31 NS083306]
- Marilyn and Frederick R. Lummis, Jr. MD Fellowship
- 2CI Neurogenomics Fellowship
- NINDS [R01 NS069828, R21 NS087360, R01 NS086082]
- National Institute of Mental Health (NIMH) [R15 MH086928]
- GSU Brains & Behavior Seed Grant
- 4-VA Innovation Award
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The basic mechanisms underlying noxious cold perception are not well understood. We developed Drosophila assays for noxious cold responses. Larvae respond to near-freezing temperatures via a mutually exclusive set of singular behaviors-in particular, a full-body contraction (CT). Class III (CIII) multidendritic sensory neurons are specifically activated by cold and optogenetic activation of these neurons elicits CT. Blocking synaptic transmission in CIII neurons inhibits CT. Genetically, the transient receptor potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII neurons, where each is required for CT. Misexpression of Pkd2 is sufficient to confer cold responsiveness. The optogenetic activation level of multimodal CIII neurons determines behavioral output, and visualization of neuronal activity supports this conclusion. Coactivation of cold-and heat-responsive sensory neurons suggests that the cold-evoked response circuitry is dominant. Our Drosophila model will enable a sophisticated molecular genetic dissection of cold nociceptive genes and circuits.
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