10:00 - 12:00
Thu-S1
Goethe Hall
Chair/s:
Friedrich Johenning, Cindy Poo
The primary olfactory (piriform) cortex receives direct input from the olfactory bulb and is a central hub for processing olfactory information. Recent evidence has suggested a role for piriform cortex in representing behaviorally relevant variables beyond odor identity. This symposium brings together researchers focused on understanding synaptic plasticity, population dynamics, and computations in piriform cortex necessary for odor-guided behaviors. The aim is to further our understanding of the functional role of the piriform cortex in complex behaviors.
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Binge eating suppresses flavor representations in the mouse olfactory cortex
Thu-S1-005
Presented by: Hung Lo
Hung Lo 1, 2, Anke Schoenherr 1, Malinda L. S. Tantirigama 3, 5, Matthew E. Larkum 3, Benjamin Judkewitz 1, 2, 5, Katharina Stumpenhorst 4, Marion Rivalan 5, York Winter 4, Dietmar Schmitz 1, 2, 5, 6, Friedrich Johenning 1, 2
1 Charité – Universitätsmedizin Berlin, Neuroscience Research Center, Berlin, Germany, 2 Einstein Center for Neurosciences Berlin, Berlin, Germany, 3 Institut für Biologie, Humboldt Universität zu Berlin, Berlin, Germany, 4 Cognitive Neurobiology, Humboldt Universität zu Berlin, Berlin, Germany, 5 NeuroCure Cluster of Excellence, Berlin, Germany, 6 Center for Neurodegenerative Diseases (DZNE), Berlin, Germany
Appropriate feeding behavior is the foundation of maintaining homeostasis. Elevated feeding rate (binge eating) is a common trait of eating disorders, and it is associated with obesity. It is also known that flavor perception has an active role in regulating feeding. However, the effects of feeding rate on flavor sensory feedback remain unknown. We developed a liquid food delivery system that mice can consume flavored milk with different feeding rates, e.g., slow eating mode (4-second interval) and binge eating mode (0.4-second interval). Using miniscope in mice, we showed that binge eating suppresses neuronal activity in the anterior olfactory (piriform) cortex (aPC), while slow eating does not. The strength of binge-induced suppression in the aPC predicts animals' consumption and duration of feeding. This suppression is unlikely due to the activation of local GABAergic interneurons (PV+ & SOM+) in the aPC. Odor inputs from olfactory bulb mitral cells remain stable upon binge eating, suggesting the suppression is not due to degraded odor inputs. We further excluded the inhibitory effect from serotonergic modulation in the aPC by using in vivo serotonin imaging. Taken together, our results provide clear circuit mechanisms of binge-induced flavor modulation, which may contribute to binge-induced overeating due to reduced sensory feedback of food items.
This project is funded by DFG 458236353.
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