Cell Reports (Feb 2022)

Escape steering by cholecystokinin peptidergic signaling

  • Lili Chen,
  • Yuting Liu,
  • Pan Su,
  • Wesley Hung,
  • Haiwen Li,
  • Ya Wang,
  • Zhongpu Yue,
  • Ming-Hai Ge,
  • Zheng-Xing Wu,
  • Yan Zhang,
  • Peng Fei,
  • Li-Ming Chen,
  • Louis Tao,
  • Heng Mao,
  • Mei Zhen,
  • Shangbang Gao

Journal volume & issue
Vol. 38, no. 6
p. 110330

Abstract

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Summary: 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.

Keywords