Articles by Heather N. Turner in JoVE
Novel Assay for Cold Nociception in Drosophila Larvae Heather N. Turner1,2,5, Christian Landry3, Michael J. Galko1,2,4 1Department of Genetics, UT MD Anderson Cancer Center, 2Neuroscience Program, Graduate School of Biomedical Sciences at Houston, 3ProDev Engineering, 4Genes and Development Program, Graduate School of Biomedical Sciences at Houston, 5Section of Neurobiology, University of Southern California Here we demonstrate a novel assay to study cold nociception in Drosophila larvae. This assay utilizes a custom-built Peltier probe capable of applying a focal noxious cold stimulus and results in quantifiable cold-specific behaviors. This technique will allow further cellular and molecular dissection of cold nociception.
Other articles by Heather N. Turner on PubMed
Macrophages Gain a Partner at the Table: Epidermal Cells Digest Peripheral Dendritic Debris in Drosophila Neuron. Feb, 2014 | Pubmed ID: 24507184 In this issue of Neuron, Han et al. (2014) develop powerful methods to visualize phagocytosis of Drosophila peripheral sensory neuron dendrites. Remarkably, epidermal cells rather than professional phagocytes are the primary mediators of debris clearance, using both familiar and new molecular players.
The TRP Channels Pkd2, NompC, and Trpm Act in Cold-Sensing Neurons to Mediate Unique Aversive Behaviors to Noxious Cold in Drosophila Current Biology : CB. Dec, 2016 | Pubmed ID: 27818173 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.