Oral Presentations and Performances: Session II
Project Type
Presentation
Project Funding and Affiliations
This project was funded by US ARO W911NF-23-1-0005 grant to SJC
Faculty Mentor’s Full Name
Sarah Certel
Faculty Mentor’s Department
Neuroscience
Additional Mentor
Erika Isern erika.isern@umconnect.umt.edu
Abstract / Artist's Statement
Gut–Brain Reprogramming Induced by Acute and Chronic Pathogen Exposures: The Role of G Protein–Coupled Receptors in Male Aggression
Kunau, J, Phillips, A, Isern, E., and Certel, S. Division of Biological Sciences, The University of Montana, Missoula, MT, United States.
Organisms must continuously interpret environmental change and rapidly adjust physiology and behavior. Ingested microbes are a powerful, understudied driver of this process because they can reshape gut to brain communication and alter behaviors such as feeding and aggression. Here we test whether acute, 24-hour ingestion of E. coli is sufficient to shift male aggression in Drosophila.
The gastrointestinal system communicates with the brain through signaling pathways that begin in the gut epithelium, where enteroendocrine cells detect nutrient and microbial cues and release peptides that influence neural circuits and behavioral state. Prior work shows that bacterial infection can alter neuromodulatory systems linked to aggression, motivating our experiments testing that microbial ingestion can change aggression thresholds.
To answer our question of whether pathogen exposure affects gut adrenergic signaling and aggression, we use Drosophila as our model system. We are comparing two exposure levels: an acute high-dose ingestion of E. coli for 24 hours and a chronic low-dose ingestion for 10 days.
After being aged to 3 days, the adult males are placed on either experimental E. coli, or two controls; heat-killed E. coli or culture medium treatment for 24 hours. We use a “Killed” E. coli treatment to see if any changes might simply be due to ingesting bacteria whether live or not. The fights are run in a standard aggression assay. Aggression is quantified using measures including latency to the first lunge and the number of lunges. Fights are scored for 20 minutes following the first lunge. If lunges do not occur within 20 minutes of pairing, the fight is excluded from analysis.
At this time, our preliminary data shows that bacteria increases latency time to fight, while our data on lunging is inconclusive. However, we are continuing to perform and score fights and will soon have enough data. These ongoing experiments will establish whether short duration microbial ingestion alters male aggression. This outcome will provide the foundation for future work testing how gut signaling mechanisms, including octopamine-mediated pathways in enteroendocrine cells, contribute to any observed behavioral shifts.
Category
Life Sciences
Gut–Brain Reprogramming Induced by Acute and Chronic Pathogen Exposures: The Role of G Protein–Coupled Receptors in Male Aggression
UC 327
Gut–Brain Reprogramming Induced by Acute and Chronic Pathogen Exposures: The Role of G Protein–Coupled Receptors in Male Aggression
Kunau, J, Phillips, A, Isern, E., and Certel, S. Division of Biological Sciences, The University of Montana, Missoula, MT, United States.
Organisms must continuously interpret environmental change and rapidly adjust physiology and behavior. Ingested microbes are a powerful, understudied driver of this process because they can reshape gut to brain communication and alter behaviors such as feeding and aggression. Here we test whether acute, 24-hour ingestion of E. coli is sufficient to shift male aggression in Drosophila.
The gastrointestinal system communicates with the brain through signaling pathways that begin in the gut epithelium, where enteroendocrine cells detect nutrient and microbial cues and release peptides that influence neural circuits and behavioral state. Prior work shows that bacterial infection can alter neuromodulatory systems linked to aggression, motivating our experiments testing that microbial ingestion can change aggression thresholds.
To answer our question of whether pathogen exposure affects gut adrenergic signaling and aggression, we use Drosophila as our model system. We are comparing two exposure levels: an acute high-dose ingestion of E. coli for 24 hours and a chronic low-dose ingestion for 10 days.
After being aged to 3 days, the adult males are placed on either experimental E. coli, or two controls; heat-killed E. coli or culture medium treatment for 24 hours. We use a “Killed” E. coli treatment to see if any changes might simply be due to ingesting bacteria whether live or not. The fights are run in a standard aggression assay. Aggression is quantified using measures including latency to the first lunge and the number of lunges. Fights are scored for 20 minutes following the first lunge. If lunges do not occur within 20 minutes of pairing, the fight is excluded from analysis.
At this time, our preliminary data shows that bacteria increases latency time to fight, while our data on lunging is inconclusive. However, we are continuing to perform and score fights and will soon have enough data. These ongoing experiments will establish whether short duration microbial ingestion alters male aggression. This outcome will provide the foundation for future work testing how gut signaling mechanisms, including octopamine-mediated pathways in enteroendocrine cells, contribute to any observed behavioral shifts.