Abstract：
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.
摘要：
逃避是一种进化上保守和必要的回避反应。被认为是天生的，大多数关于逃避反应的研究集中在硬连线电路上。我们在此报告，神经肽NLP-18及其胆囊收缩素受体CKR-1使逃逸电路能够执行完整的omega（Ω）转弯。我们证明了体内NLP-18主要由味觉感觉神经元（ASI）分泌，以激活头运动神经元（SMD）和转角启动中间神经元（AIB）中的CKR-1。在SMD或AIB神经元中NLP-18或CKR-1的去除或CKR-1的特异性敲低导致较浅的转弯，因此不那么强大的逃生转向。始终如一，消除NLP-18或CKR-1后，逃避转向过程中头部运动神经元（SMD）的Ca2瞬变的升高会减弱。体外，合成的NLP-18直接引起卵母细胞中CKR-1依赖性电流和SMD中CKR-1依赖性Ca2瞬变。因此，胆囊收缩素肽能信号调节逃逸回路以产生强大的逃逸转向。
