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

Date of Award

Summer 2015

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Department of Biology

Advisor(s)

Susan R. Halsell

Abstract

The reflexive response and perception of pain (nociception) is an evolutionarily conserved process in animals. Pain can be a major health concern and current treatments often prove insufficient, especially in regards to chronic pain. Greater understanding of the molecular processes underlying pain sensation could lead to new and more effective treatments. The aim of this study is to investigate the molecular mechanisms of cold nociception in Drosophila melanogaster. A specific subset of peripheral sensory neurons (Class III dendritic arborization (da) neurons), are implicated in Drosophila larvae’s response to noxious cold.

Previous literature has implicated a variety of ion channel families, including transient receptor potential (TRP) and degenerin/epithelial sodium channels (DEG/ENaC) family members, in mediating sensory responses to noxious heat and mechanosensation. Though much is known about noxious mechanical and heat nociception in Drosophila, little is known regarding the molecular components mediating cold nociception.

Here we focus on characterization of Drosophila DEG/ENaC family members as potential regulators of noxious cold-evoked sensory behavior. A novel behavioral assay, coupled with functional optogenetic studies and in vivo RNAi expression, has been utilized to investigate the role of select pickpocket (ppk) family members. Our analyses reveal that ppk12, ppk23, and ppk25 are required for noxious cold detection in larvae. These studies provide novel mechanistic insight into the molecular underpinnings of cold-evoked behavioral responses and demonstrate a previously uncharacterized function for DEG/ENaC molecules in cold nociception.

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