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.

能量感应神经回路决定消耗或节省资源，部分是基于它们接收到的滋补、稳态、能量存储信息。以脂肪组织来源的脂肪因子形式存在的强直信号设定了能量感应神经元的基线活动水平，从而为解释额外输入提供了背景。然而，强直脂肪因子信息建立稳态神经元功能的机制迄今尚不清楚。我们在这里表明，在营养过剩的条件下，Upd2，一种果蝇瘦素直向同源物调节基于肌动蛋白的突触重组以减少抑制回路中的布顿数，从而建立允许胰岛素释放的神经张力。出乎意料的是，我们发现胰岛素反馈到这些相同的抑制性神经元，反过来增加布顿数，导致维持负音。我们的结果指出了一种机制，通过该机制，两个剩余感知激素系统 Upd2/瘦素和胰岛素会聚在具有相反结果的神经元回路上，以建立依赖于能量储存的神经元活动。