Cell type-specific contributions to a persistent aggressive internal state in female Drosophila
Creators
Abstract
Persistent internal states are important for maintaining survival-promoting behaviors, such as aggression. In female Drosophila melanogaster, we have previously shown that individually activating either aIPg or pC1d cell types can induce aggression. Here we investigate further the individual roles of these cholinergic, sexually dimorphic cell types, and the reciprocal connections between them, in generating a persistent aggressive internal state. We find that a brief 30-second optogenetic stimulation of aIPg neurons was sufficient to promote an aggressive internal state lasting at least 10 minutes, whereas similar stimulation of pC1d neurons did not. While we previously showed that stimulation of pC1e alone does not evoke aggression, persistent behavior could be promoted through simultaneous stimulation of pC1d and pC1e, suggesting an unexpected synergy of these cell types in establishing a persistent aggressive state. Neither aIPg nor pC1d show persistent neuronal activity themselves, implying that the persistent internal state is maintained by other mechanisms. Moreover, inactivation of pC1d did not significantly reduce aIPg-evoked persistent aggression, arguing that the aggressive state did not depend on pC1d-aIPg recurrent connectivity. Our results suggest the need for alternative models to explain persistent female aggression.
Copyright and License
© 2023, Chiu et al. Subject to a Creative Commons Attribution license, except where otherwise noted.
Data Availability
Data is included in the paper and the supplementary files. Source data have been provided for Figures 2 and 4, Figure 2—figure supplements 1 and 2, Figure 3—figure supplement 1, Figure 4—figure supplement 1. Source code was adapted from Chiu et al., 2021 and is available in GitHub (copy archived at Chiu and Schretter, 2025).
Funding
Howard Hughes Medical Institute
National Institutes of Health (R37DA031389)
Acknowledgement
We thank M Dreher (Dreher Design Studio) for help with connectomics figures; A Sanchez (Caltech) for fly maintenance; C Chiu, G Mancuso, L Chavarria, X Da (Caltech), and A Howard (Janelia) for laboratory management and administrative assistance; and Dr D Bushey (Janelia) for help with additional calcium imaging experiments. We also thank Drs D Deutsch, D Galili, U Heberlein, M Murthy, and A Otopalik for their helpful feedback on the manuscript as well as the broader Janelia community for their suggestions throughout this work.
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Additional details
Funding
- Howard Hughes Medical Institute
- National Institutes of Health
- R37DA031389
Dates
- Available
-
2025-07-25Version of record