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Celsr3驱动听觉惊吓后脑回路的发育和连接。

Celsr3 drives development and connectivity of the acoustic startle hindbrain circuit.

作者信息

Meserve Joy H, Navarro Maria F, Ortiz Elelbin A, Granato Michael

机构信息

Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.

出版信息

bioRxiv. 2024 Mar 7:2024.03.07.583806. doi: 10.1101/2024.03.07.583806.

Abstract

In the developing brain, groups of neurons organize into functional circuits that direct diverse behaviors. One such behavior is the evolutionarily conserved acoustic startle response, which in zebrafish is mediated by a well-defined hindbrain circuit. While numerous molecular pathways that guide neurons to their synaptic partners have been identified, it is unclear if and to what extent distinct neuron populations in the startle circuit utilize shared molecular pathways to ensure coordinated development. Here, we show that the planar cell polarity (PCP)-associated atypical cadherins Celsr3 and Celsr2, as well as the Celsr binding partner Frizzled 3a/Fzd3a, are critical for axon guidance of two neuron types that form synapses with each other: the command-like neuron Mauthner cells that drive the acoustic startle escape response, and spiral fiber neurons which provide excitatory input to Mauthner cells. We find that Mauthner axon growth towards synaptic targets is vital for Mauthner survival. We also demonstrate that symmetric spiral fiber input to Mauthner cells is critical for escape direction, which is necessary to respond to directional threats. Moreover, we identify distinct roles for Celsr3 and Celsr2, as Celsr3 is required for startle circuit development while Celsr2 is dispensable, though Celsr2 can partially compensate for loss of Celsr3 in Mauthner cells. This contrasts with facial branchiomotor neuron migration in the hindbrain, which requires Celsr2 while we find that Celsr3 is dispensable. Combined, our data uncover critical and distinct roles for individual PCP components during assembly of the acoustic startle hindbrain circuit.

摘要

在发育中的大脑中,神经元群体会组织成指导各种行为的功能回路。其中一种行为是进化上保守的听觉惊吓反应,在斑马鱼中,这种反应由一个明确的后脑回路介导。虽然已经确定了许多引导神经元与其突触伙伴连接的分子途径,但尚不清楚惊吓回路中不同的神经元群体是否以及在何种程度上利用共享的分子途径来确保协调发育。在这里,我们表明,平面细胞极性(PCP)相关的非典型钙黏蛋白Celsr3和Celsr2,以及Celsr结合伴侣卷曲蛋白3a/Fzd3a,对于两种相互形成突触的神经元类型的轴突导向至关重要:驱动听觉惊吓逃逸反应的指令样神经元毛特纳细胞,以及向毛特纳细胞提供兴奋性输入的螺旋纤维神经元。我们发现毛特纳轴突向突触靶点的生长对毛特纳细胞的存活至关重要。我们还证明,毛特纳细胞的对称螺旋纤维输入对于逃逸方向至关重要,而逃逸方向对于应对定向威胁是必要的。此外,我们确定了Celsr3和Celsr2的不同作用,因为惊吓回路发育需要Celsr3,而Celsr2是可有可无的,尽管Celsr2可以部分补偿毛特纳细胞中Celsr3的缺失。这与后脑的面部鳃运动神经元迁移形成对比,后脑的面部鳃运动神经元迁移需要Celsr2,而我们发现Celsr3是可有可无的。综合来看,我们的数据揭示了在听觉惊吓后脑回路组装过程中,单个PCP组件的关键和不同作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a7a/10942420/feb0ea1bb692/nihpp-2024.03.07.583806v1-f0001.jpg

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