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通过肽能信号的基因操纵重新安排固定行为模式的行为亚单位。

Rescheduling Behavioral Subunits of a Fixed Action Pattern by Genetic Manipulation of Peptidergic Signaling.

作者信息

Kim Do-Hyoung, Han Mi-Ran, Lee Gyunghee, Lee Sang Soo, Kim Young-Joon, Adams Michael E

机构信息

Department of Entomology, University of California, Riverside, Riverside, California, United States of America.

Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, South Korea.

出版信息

PLoS Genet. 2015 Sep 24;11(9):e1005513. doi: 10.1371/journal.pgen.1005513. eCollection 2015 Sep.

DOI:10.1371/journal.pgen.1005513
PMID:26401953
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4581697/
Abstract

The ecdysis behavioral sequence in insects is a classic fixed action pattern (FAP) initiated by hormonal signaling. Ecdysis triggering hormones (ETHs) release the FAP through direct actions on the CNS. Here we present evidence implicating two groups of central ETH receptor (ETHR) neurons in scheduling the first two steps of the FAP: kinin (aka drosokinin, leucokinin) neurons regulate pre-ecdysis behavior and CAMB neurons (CCAP, AstCC, MIP, and Bursicon) initiate the switch to ecdysis behavior. Ablation of kinin neurons or altering levels of ETH receptor (ETHR) expression in these neurons modifies timing and intensity of pre-ecdysis behavior. Cell ablation or ETHR knockdown in CAMB neurons delays the switch to ecdysis, whereas overexpression of ETHR or expression of pertussis toxin in these neurons accelerates timing of the switch. Calcium dynamics in kinin neurons are temporally aligned with pre-ecdysis behavior, whereas activity of CAMB neurons coincides with the switch from pre-ecdysis to ecdysis behavior. Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is sufficient to trigger ecdysis behavior. Our findings demonstrate that kinin and CAMB neurons are direct targets of ETH and play critical roles in scheduling successive behavioral steps in the ecdysis FAP. Moreover, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.

摘要

昆虫的蜕皮行为序列是一种由激素信号引发的经典固定动作模式(FAP)。蜕皮触发激素(ETHs)通过直接作用于中枢神经系统来释放FAP。在此,我们提供证据表明两组中枢ETH受体(ETHR)神经元在安排FAP的前两个步骤中发挥作用:激肽(又名果蝇激肽、亮氨酸激肽)神经元调节蜕皮前行为,而CAMB神经元(CCAP、AstCC、MIP和bursicon)启动向蜕皮行为的转变。激肽神经元的消融或这些神经元中ETH受体(ETHR)表达水平的改变会改变蜕皮前行为的时间和强度。CAMB神经元的细胞消融或ETHR基因敲低会延迟向蜕皮行为的转变,而这些神经元中ETHR的过表达或百日咳毒素的表达则会加速转变的时间。激肽神经元中的钙动力学在时间上与蜕皮前行为一致,而CAMB神经元的活动则与从蜕皮前行为向蜕皮行为的转变相吻合。通过温度敏感的TRPM8门控激活CCAP或CAMB神经元足以触发蜕皮行为。我们的研究结果表明,激肽和CAMB神经元是ETH的直接靶点,在安排蜕皮FAP中连续的行为步骤中起关键作用。此外,FAP的时间组织可能是靶神经元中ETH受体密度的函数。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/ef98a88896b1/pgen.1005513.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/0759a32cb9c7/pgen.1005513.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/79cf19642d08/pgen.1005513.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/2c96974cd4c8/pgen.1005513.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/f4b06f3bdcc7/pgen.1005513.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/c93dba0d890d/pgen.1005513.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/ef98a88896b1/pgen.1005513.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/0759a32cb9c7/pgen.1005513.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/815784f5fb10/pgen.1005513.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/79cf19642d08/pgen.1005513.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/2c96974cd4c8/pgen.1005513.g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/c93dba0d890d/pgen.1005513.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c680/4581697/ef98a88896b1/pgen.1005513.g007.jpg

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