Chronic pain affects approximately 100 million Americans and generates costs of up to $600 billion per year, according to the Institute of Medicine. Characterization of molecular signaling pathways in sensory neurons is an important step toward development of more effective clinical interventions. The goal of this study is to identify genes involved in regulating the function of class IV multidendritic neurons, which are nociceptors integral to the detection of noxious thermal, mechanical, and photic stimuli. We are using Drosophila melanogaster larvae as a model system, which exhibit a distinct and quantifiable response to noxious stimuli termed nocifensive escape locomotion (NEL). Recent research has found that the transcripts of key genes necessary for nociceptor function are alternatively spliced. We have systematically knocked down putative RNA-processing genes with a previously identified role in dendrite development and/or alternative splicing by crossing a ppk-GAL4;UAS-dicer2 fly strain with RNAi lines targeting genes of interest. Using ppk-GAL4 as our driver limits expression to nociceptors and dicer2 expression promotes increased efficacy of RNAi knockdown. We then tested progeny for changes in NEL latency relative to wild-type larvae using a thermal nociception assay. Nineteen genes were identified for which knockdown resulted in either a significant increase or decrease in response latency, indicating a potential defect. Follow-up assays for defects in mechanical nociception have demonstrated that select genes are required for both thermal and mechanical nociception. Additionally, our results suggest that behavioral defects do not always correlate with defects in dendrite morphology. This study has also revealed a complex role for translation initiation factors, which will be investigated further using genetic and functional assays of multidendritic neuron structure and function.