Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Date of Graduation

5-8-2020

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Department of Biology

Advisor(s)

Susan Halsell

Corey Cleland

Marquis Walker

Abstract

Nociception is an organism’s ability to detect, process and reflexively respond to potentially damaging stimuli. While the process of nociception has clear, protective advantages, inappropriate and prolonged signaling can lead to chronic pain in humans. Nociception is a vital and genetically conserved process, thus cold nociception in Drosophilaprovides a model for identifying molecular components required for nociceptor function in vertebrates. Drosophila Class III dendritic arborization (da) neurons have previously been shown to be involved in the cold nociceptive response. Due to the importance of fast response to damaging stimuli, we hypothesize that electrical synapses are involved in cold nociception. Structurally, electrical synapses are gap junctions, and Innexins form gap junctions. Eight genes comprise the innexin gene family in Drosophila. In this study the expression and functionality of each innexin has been analyzed by RNAi knock down or with a loss-of-function ogre (inx1) mutant was also analyzed. Functionality was assessed with a cold behavioral assay. The wild-type Drosophila larvae exhibit a full body cringe response is easily quantified in these assays. Statistical comparison of the number of cringers for the RNAi knockdown of an innexin and its experimental control gave insight into an innexins potential involvement in cold nociception. By comparing the behavioral data and the expression data the innexins that are the strongest candidates for cold nociception function are ogre (inx1), inx2, zpg(inx4), inx5 and shakB (inx8). Future studies will further characterize these innexins role in cold nociception.

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