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Insulin receptor signaling in sugar-sensing gustatory neurons impacts "sweet" sensitivity

Arntsen, Christian
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Abstract
Previous work in Drosophila melanogaster demonstrates that taste cells are directly impacted by starvation to increase the palatability of sugars. The cellular and molecular mechanisms underlying this modulation remain unclear, specifically the role of canonical satiety hormones like insulin. Therefore, we manipulated insulin receptor signaling only in sugar-sensing GRNs. Inactive insulin signaling resulted in increased sucrose sensitivity and taste cell activation, specifically in the fed state. Overactive insulin signaling did not impact behavior but resulted in suppressed neuronal activation in the starved state. Overall, we conclude that InR signaling in sugar-sensing GRNs impacts ‘sweet’ sensitivity in a state-dependent manner.
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Date
2024-01-01
Student Status
Graduate
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Poster Presentation
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UVM Student Research Conference
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https://hdl.handle.net/20.500.14849/8765
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Advisor(s)
Molly Stanley
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Program/Major
Neuroscience
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Graduate College
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Life Sciences
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