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Updated: Jun 23, 2026
An Improved Assay and Tools for Measuring Mechanical Nociception in Drosophila Larvae
Published on: October 29, 2020
Cytokine signaling mediates UV-induced nociceptive sensitization in Drosophila larvae
Daniel T Babcock1, Christian Landry, Michael J Galko
1Department of Biochemistry and Molecular Biology, University of Texas Graduate School of Biomedical Sciences, USA.
Background:
Heightened nociceptive (pain) sensitivity is an adaptive response to tissue damage and serves to protect the site of injury. Multiple mediators of nociceptive sensitization have been identified in vertebrates, but the complexity of the vertebrate nervous system and tissue-repair responses has hindered identification of the precise roles of these factors.
Results:
Here we establish a new model of nociceptive sensitization in Drosophila larvae, in which UV-induced tissue damage alters an aversive withdrawal behavior. We find that UV-treated larvae develop both thermal hyperalgesia, manifested as an exaggerated response to noxious thermal stimuli, and thermal allodynia, a responsiveness to subthreshold thermal stimuli that are not normally perceived as noxious. Allodynia is dependent upon a tumor necrosis factor (TNF) homolog, Eiger, released from apoptotic epidermal cells, and the TNF receptor, Wengen, expressed on nociceptive sensory neurons.
Conclusions:
These results demonstrate that cytokine-mediated nociceptive sensitization is conserved across animal phyla and set the stage for a sophisticated genetic dissection of the cellular and molecular alterations responsible for development of nociceptive sensitization in sensory neurons.
Insights
This study reveals that UV-induced tissue damage in Drosophila larvae causes heightened pain sensitivity, including thermal hyperalgesia and allodynia. This pain sensitization is mediated by a tumor necrosis factor (TNF) pathway, conserved across species.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Heightened nociceptive (pain) sensitivity is an adaptive response to tissue damage.
- The complexity of vertebrate systems has hindered understanding of pain mediator roles.
Purpose of the Study:
- Establish a new model for studying nociceptive sensitization in Drosophila larvae.
- Investigate the mechanisms underlying UV-induced pain sensitization.
Main Methods:
- UV-induced tissue damage in Drosophila larvae.
- Behavioral analysis of thermal hyperalgesia and allodynia.
- Genetic analysis of the tumor necrosis factor (TNF) pathway.
Main Results:
- UV-treated larvae exhibit exaggerated responses to noxious heat (hyperalgesia) and respond to normally non-painful stimuli (allodynia).
- Allodynia is dependent on Eiger, a TNF homolog released from damaged cells.
- Wengen, a TNF receptor on sensory neurons, is crucial for allodynia.
Conclusions:
- Cytokine-mediated nociceptive sensitization is conserved across animal phyla.
- This model allows for genetic dissection of pain sensitization mechanisms in sensory neurons.
