Escape steering by cholecystokinin peptidergic signaling
| Autor: | 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 |
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| Rok vydání: | 2021 |
| Předmět: |
Sensory Receptor Cells
CKR-1 QH301-705.5 Neuropeptides cholecystokinin receptor NLP-18 General Biochemistry Genetics and Molecular Biology neuromodulator Animals escape Biology (General) Caenorhabditis elegans Caenorhabditis elegans Proteins Cholecystokinin neuropeptide Locomotion Signal Transduction |
| Zdroj: | Cell Reports, Vol 38, Iss 6, Pp 110330-(2022) |
| ISSN: | 2211-1247 |
| Popis: | 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 peptidergic signaling is an integral and necessary component of the Caenorhabditis elegans escape circuit. Combining genetic screening, electrophysiology and calcium imaging, we reveal that a neuropeptide NLP-18 and its cholecystokinin receptor CKR-1 enable the escape circuit to execute a full omega (Ω) turn, the last motor step where the animal robustly steers away from its original trajectory. We demonstrate in vivo and in vitro that CKR-1 is a Gαq protein coupled receptor for NLP-18. 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, removal of CKR-1, or specific knockdown of CKR-1 in SMD or AIB neurons lead 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 signaling modulates an escape circuit to generate robust escape steering. |
| Databáze: | OpenAIRE |
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