%0 Journal Article
%T Escape steering by cholecystokinin peptidergic signaling.
%A Chen L
%A Liu Y
%A Su P
%A Hung W
%A Li H
%A Wang Y
%A Yue Z
%A Ge MH
%A Wu ZX
%A Zhang Y
%A Fei P
%A Chen LM
%A Tao L
%A Mao H
%A Zhen M
%A Gao S
%J Cell Rep
%V 38
%N 6
%D 02 2022 8
%M 35139370
暂无%R 10.1016/j.celrep.2022.110330
%X 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 Ca2+ 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 Ca2+ transients in SMD. Thus, cholecystokinin peptidergic signaling modulates an escape circuit to generate robust escape steering.