基于 TEM 研究的 Neurexin 和 Neuroligins 共同调节果蝇神经肌肉接头处的突触变性,Frontiers in Cellular Neuroscience

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基于 TEM 研究的 Neurexin 和 Neuroligins 共同调节果蝇神经肌肉接头处的突触变性
Frontiers in Cellular Neuroscience ( IF 4.2 ) Pub Date : 2023-11-01 , DOI: 10.3389/fncel.2023.1257347
Gan Guangming _{1,

2} , Chen Mei ₂ , Yu Qinfeng ₁ , Gao Xiang ₁ , Zhang Chenchen ₁ , Sheng Qingyuan ₂ , Xie Wei _{2,

3} , Geng Junhua _{2,

4}

Affiliation

这果蝇幼虫神经肌肉接头（NMJ）是众所周知的模型系统，经常用于研究突触发育。在这里，我们主要基于透射电子显微镜 (TEM) 研究，展示了 NMJ 突触变性。当退化开始时，突触下网（SSR）膨胀、收缩并向内折叠，残余的 SSR 然后退化成无序的、薄的或线性的膜。轴突末梢从中心区域开始退化，T形杆与突触前膜脱离，突触小泡聚集，加速大规模退化。透明突触小泡有两种变性模式。在第一种模式中，没有肌动蛋白丝的突触小泡在膜上退化，具有超细斑点，并塌陷和分散，形成具有深色超细颗粒的不规则轮廓。在第二种模式中，具有肌动蛋白丝的透明突触小泡退化为致密突触小泡，形成不规则的无膜深色团块，并塌陷和分散形成带有深色超细颗粒的不规则轮廓。最后，NMJ 扣中的所有残留膜退化为线性形状，轴突末端的所有残留元素退化并最终形成一团黑色超细颗粒。SSR 的肿胀和回缩发生在轴突末端退化之前，轴突末端比 SSR 退化更快且强度更大。NMJ bouton 变性在正常生理条件下发生，但在果蝇神经毒素（DNRX）DNRX273,果蝇神经胶质素（DNLG）dnlg1和dnlg4突变体和DNRX83;dnlg3和dnlg2;dnlg3双突变体，这表明神经毒素和神经连接蛋白在预防突触变性中发挥着至关重要的作用。

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Neurexin and neuroligins jointly regulate synaptic degeneration at the Drosophila neuromuscular junction based on TEM studies

The Drosophila larval neuromuscular junction (NMJ) is a well-known model system and is often used to study synapse development. Here, we show synaptic degeneration at NMJ boutons, primarily based on transmission electron microscopy (TEM) studies. When degeneration starts, the subsynaptic reticulum (SSR) swells, retracts and folds inward, and the residual SSR then degenerates into a disordered, thin or linear membrane. The axon terminal begins to degenerate from the central region, and the T-bar detaches from the presynaptic membrane with clustered synaptic vesicles to accelerate large-scale degeneration. There are two degeneration modes for clear synaptic vesicles. In the first mode, synaptic vesicles without actin filaments degenerate on the membrane with ultrafine spots and collapse and disperse to form an irregular profile with dark ultrafine particles. In the second mode, clear synaptic vesicles with actin filaments degenerate into dense synaptic vesicles, form irregular dark clumps without a membrane, and collapse and disperse to form an irregular profile with dark ultrafine particles. Last, all residual membranes in NMJ boutons degenerate into a linear shape, and all the residual elements in axon terminals degenerate and eventually form a cluster of dark ultrafine particles. Swelling and retraction of the SSR occurs prior to degradation of the axon terminal, which degenerates faster and with more intensity than the SSR. NMJ bouton degeneration occurs under normal physiological conditions but is accelerated in Drosophila neurexin (dnrx) dnrx273, Drosophila neuroligin (dnlg) dnlg1 and dnlg4 mutants and dnrx83;dnlg3 and dnlg2;dnlg3 double mutants, which suggests that both neurexin and neuroligins play a vital role in preventing synaptic degeneration.

更新日期：2023-11-01

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