Electrical synapses are specialized structures that mediate the flow of electrical currents between neurons and have well known roles in synchronizing the activities of neuronal populations, both by mediating the current transfer from more active to less active neurons and by shunting currents from active neurons to their less active neighbors. However, how these positive and negative functions of electrical synapses are coordinated to shape rhythmic synaptic outputs and behavior is not well understood. Here, using a combination of genetics, behavioral analysis, and live calcium imaging in Caenorhabditis elegans, we show that electrical synapses formed by the gap junction protein INX-1/innexin couple the presynaptic terminals of a pair of motor neurons (AVL and DVB) to synchronize their activation in response to a pacemaker signal. Live calcium imaging reveals that inx-1/innexin mutations lead to asynchronous activation of AVL and DVB, due, in part, to loss of AVL-mediated activation of DVB by the pacemaker. In addition, loss of inx-1 leads to the ectopic activation of DVB at inappropriate times during the cycle through the activation of the L-type voltage-gated calcium channel EGL-19. We propose that electrical synapses between AVL and DVB presynaptic terminals function to ensure the precise and robust execution of a specific step in a rhythmic behavior by both synchronizing the activities of presynaptic terminals in response to pacemaker signaling and by inhibiting their activation in between cycles when pacemaker signaling is low.

电突触是调节神经元之间电流流动的特殊结构，在同步神经元群的活动方面具有众所周知的作用，既通过介导电流从较活跃的神经元转移到较不活跃的神经元，也通过将电流从活跃的神经元分流到较不活跃的神经元活跃的邻居。然而，电突触的这些积极和消极功能如何协调以形成有节奏的突触输出和行为尚不清楚。在这里，在秀丽隐杆线虫中使用遗传学、行为分析和活钙成像的组合，我们显示由间隙连接蛋白 INX-1/innexin 形成的电突触耦合一对运动神经元（AVL 和 DVB）的突触前末梢，以同步它们响应起搏器信号的激活。实时钙成像显示inx-1 / innexin突变导致 AVL 和 DVB 的异步激活，部分原因是起搏器对 AVL 介导的 DVB 激活的丧失。此外，inx-1 的损失通过激活 L 型电压门控钙通道 EGL-19，导致 DVB 在循环期间的不适当时间异位激活。我们建议 AVL 和 DVB 突触前末梢之间的电突触通过同步突触前末梢响应起搏器信号的活动以及在起搏器发出信号时抑制它们的激活来确保节律行为中特定步骤的精确和稳健执行。信号低。