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Drosulfakinin 信号调节 在 中的雌性性接受性。

Drosulfakinin signaling modulates female sexual receptivity in .

机构信息

School of Life Sciences, University of Science and Technology of China, Hefei, China.

State Key Laboratory of Integrated Management of Pest Insects and Rodents Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

出版信息

Elife. 2022 Apr 27;11:e76025. doi: 10.7554/eLife.76025.

Abstract

Female sexual behavior as an innate behavior is of prominent biological importance for survival and reproduction. However, molecular and circuit mechanisms underlying female sexual behavior is not well understood. Here, we identify the Cholecystokinin-like peptide Drosulfakinin (DSK) to promote female sexual behavior in . Loss of DSK function reduces female receptivity while overexpressing DSK enhances female receptivity. We identify two pairs of -expressing neurons in the central brain to promote female receptivity. We find that the DSK peptide acts through one of its receptors, CCKLR-17D3, to modulate female receptivity. Manipulation of CCKLR-17D3 and its expressing neurons alters female receptivity. We further reveal that the two pairs of -expressing neurons receive input signal from pC1 neurons that integrate sex-related cues and mating status. These results demonstrate how a neuropeptide pathway interacts with a central neural node in the female sex circuitry to modulate sexual receptivity.

摘要

雌性性行为作为一种先天行为,对生存和繁殖具有突出的生物学重要性。然而,雌性性行为的分子和回路机制尚不清楚。在这里,我们鉴定出胆囊收缩素样肽 Drosulfakinin(DSK)可促进 中的雌性性行为。DSK 功能缺失会降低雌性接受度,而过表达 DSK 则会增强雌性接受度。我们鉴定出中央脑中两对表达的神经元可促进雌性接受度。我们发现 DSK 肽通过其受体之一 CCKLR-17D3 发挥作用,从而调节雌性接受度。操纵 CCKLR-17D3 及其表达神经元会改变雌性接受度。我们进一步揭示出这两对表达的神经元接收来自 pC1 神经元的输入信号,这些神经元整合了与性相关的线索和交配状态。这些结果表明,神经肽途径如何与雌性性电路中的中央神经节点相互作用以调节性接受度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5fe/9045819/2cef2afcc1fa/elife-76025-fig1.jpg

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