Insulin and Leptin/Upd2 Exert Opposing Influences on Synapse Number in Fat-Sensing Neurons
| Autor: | Ava E. Brent, Akhila Rajan |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Leptin
0301 basic medicine Physiology medicine.medical_treatment Adipokine Biology Inhibitory postsynaptic potential Article Energy homeostasis Tonic (physiology) Fats 03 medical and health sciences 0302 clinical medicine medicine Biological neural network Animals Drosophila Proteins Insulin Molecular Biology Neurons Cell Biology Drosophila melanogaster 030104 developmental biology medicine.anatomical_structure nervous system Synapses Neuron Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Cell Metab |
| ISSN: | 1550-4131 |
| DOI: | 10.1016/j.cmet.2020.08.017 |
| Popis: | Summary 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. |
| Databáze: | OpenAIRE |
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