Homeostatic synaptic plasticity (HSP) involves compensatory mechanisms employed by neurons and circuits to preserve signaling when confronted with global changes in activity that may occur during physiological and pathological conditions. Cholinergic neurons, which are especially affected in some pathologies, have recently been shown to exhibit HSP mediated by nicotinic acetylcholine receptors (nAChRs). In Drosophila central neurons, pharmacological blockade of activity induces a homeostatic response mediated by the Drosophila α7 (Dα7) nAChR, which is tuned by a subsequent increase in expression of the voltage-dependent K_v4/Shal channel. Here, we show that an in vivo reduction of cholinergic signaling induces HSP mediated by Dα7 nAChRs, and this upregulation of Dα7 itself is sufficient to trigger transcriptional activation, mediated by nuclear factor of activated T cells (NFAT), of the K_v4/Shal gene, revealing a receptor-ion channel system coupled for homeostatic tuning in cholinergic neurons.

稳态突触可塑性（HSP）涉及神经元和回路采用的补偿机制，当在生理和病理条件下可能发生的整体活动变化时，可以保留信号。胆碱能神经元，特别是在某些病理中受到影响，最近已显示出由烟碱乙酰胆碱受体（nAChRs）介导的热休克蛋白。在果蝇中枢神经元中，药理活性的阻断诱导了由果蝇α7（Dα7）nAChR介导的体内稳态反应，该反应可通过随后依赖电压依赖性K _v 4 / Shal通道表达的增加来调节。在这里，我们展示了一种体内胆碱能信号传导的减少会诱导Dα7nAChRs介导的HSP，而Dα7本身的这种上调足以触发K _v 4 / Shal基因的活化T细胞核因子（NFAT）介导的转录激活，从而揭示受体离子。通道系统耦合胆碱能神经元的稳态调节。