Journal
CELL METABOLISM
Volume 32, Issue 5, Pages 786-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2020.08.017
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Funding
- NIH Cancer Center Support Grant [P30 CA015704]
- NIH [2P40OD010949]
- Bloomington Drosophila Stock Center [NIH P40OD018537]
- Transgenic RNAi Resource project [NIGMS R01 GM084947, NIGMSP41 GM132087]
- HHMI-EXORP
- NIDDK [R00DK101605]
- NIGMS [R35GM124593]
- Hearst Foundation
- Fred Hutch New Development Funds
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Energy-sensing neural circuits decide to expend or conserve resources based, in part, on the tonic, steady-state, energy-store information they receive. Tonic signals, in the form of adipose tissue-derived adipokines, set the baseline level of activity in the energy-sensing neurons, thereby providing context for interpretation of additional inputs. However, the mechanism by which tonic adipokine information establishes steady-state neuronal function has heretofore been unclear. We show here that under conditions of nutrient surplus, Upd2, a Drosophila leptin ortholog, regulates actin-based synapse reorganization to reduce bouton number in an inhibitory circuit, thus establishing a neural tone that is permissive for insulin release. Unexpectedly, we found that insulin feeds back on these same inhibitory neurons to conversely increase bouton number, resulting in maintenance of negative tone. Our results point to a mechanism by which two surplus-sensing hormonal systems, Upd2/leptin and insulin, converge on a neuronal circuit with opposing outcomes to establish energy-store-dependent neuron activity.
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