Summary
Energy sensing neural circuits decide to expend or conserve resources by integrating tonic steady-state energy store information with phasic signals for hunger and food intake. Tonic signals, in the form of adipose tissue-derived adipokines, set the baseline level of energy-sensing neuron activity, providing context for interpretation of phasic messages. However, the mechanism by which tonic adipokine information establishes baseline neuronal function is unclear. Here we show that Upd2, a Drosophila Leptin ortholog, regulates actin-based synapse reorganization by reducing inhibitory synaptic contacts, thereby providing a permissive neural tone for insulin release under conditions of nutrient surplus. Unexpectedly, Insulin acts on the same upstream inhibitory neurons to conversely increase synapse number, hence re-instating negative tone. Our results suggest that two surplus-sensing hormonal systems, Leptin/Upd2 and Insulin, converge on a neuronal circuit with opposing outcomes that establish tonic, energy-store-dependent neuron activity.
Highlights
The adipokine Upd2 regulates number of inhibitory synaptic contacts on Insulin neurons.
Upd2 activates an actin-regulating complex of Arouser, Basigin, and Gelsolin in target neurons.
Arouser, Basigin, and Gelsolin reduce the extent of inhibitory contact on Insulin neurons.
Insulin resets negative tone by increasing the number of synaptic contacts made by its own upstream inhibitory neurons.
