Escape steering by cholecystokinin peptidergic signaling

作者：Lili Chen, Yuting Liu, Pan Su, Wesley Hung, Haiwen Li, Ya Wang, Zhongpu Yue, Ming-Hai Ge, Zheng‐Xing Wu, Yan Zhang, Peng Fei, Liming Chen, Louis Tao, Heng Mao, Mei Zhen, Shangbang Gao · 发表于：Cell Reports · 年份：2022 · DOI：10.1016/j.celrep.2022.110330 · 被引用次数：28 · 研究领域：Circadian rhythm and melatonin、Neurobiology and Insect Physiology Research、Photoreceptor and optogenetics research

Escape is an evolutionarily conserved and essential avoidance response. Considered to be innate, most studies on escape responses focused on hard-wired circuits. We report here that a neuropeptide NLP-18 and its cholecystokinin receptor CKR-1 enable the escape circuit to execute a full omega (Ω) turn. We demonstrate in vivo NLP-18 is mainly secreted by the gustatory sensory neuron (ASI) to activate CKR-1 in the head motor neuron (SMD) and the turn-initiating interneuron (AIB). Removal of NLP-18 or CKR-1 or specific knockdown of CKR-1 in SMD or AIB neurons leads to shallower turns, hence less robust escape steering. Consistently, elevation of head motor neuron (SMD)'s Ca 2+ transients during escape steering is attenuated upon the removal of NLP-18 or CKR-1. In vitro , synthetic NLP-18 directly evokes CKR-1-dependent currents in oocytes and CKR-1-dependent Ca 2+ transients in SMD. Thus, cholecystokinin peptidergic signaling modulates an escape circuit to generate robust escape steering.