Newly synthesized proteins support the development of functional neural circuits and previous work has suggested that dysregulated translation mediates certain forms of autism spectrum disorder (ASD). Here, we investigated the role of Target of Rapamycin Complex 1 (TORC1) in synaptic and dendritic development in vivo in the retinotectal system of Xenopus laevis tadpoles. We found that TORC1 signaling regulates dendritic growth and branching and that acute over‐activation of TORC1 by Rheb overexpression drove enhanced maturation of excitatory synapses by recruiting AMPA receptors. Interestingly, TORC1 over‐activation did not affect inhibitory transmission, resulting in a significant imbalance in the excitatory‐to‐inhibitory ratio. Rheb overexpression also enlarged excitatory visual input fields in tectal neurons, consistent with dysregulation of retinotopic input refinement and integration of the cell into the circuit. In contrast to other reports that mainly found impairments in synaptic inhibition using broad systemic deletion or mutation of TORC1 regulatory proteins, our findings from acute, local manipulation of TORC1 reveal its critical role in selectively regulating the number and maturity of excitatory, but not inhibitory, synapses in the developing brain.

中文翻译：

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TORC1选择性调节发育中的视觉系统中的突触成熟和输入收敛

新合成的蛋白质支持功能性神经回路的发展，之前的工作表明翻译失调介导某些形式的自闭症谱系障碍 (ASD)。在这里，我们研究了雷帕霉素靶标复合物 1 (TORC1) 在非洲爪蟾视网膜系统 体内 突触和树突发育中的作用蝌蚪。我们发现TORC1信号调节树突生长和分支，并且Rheb过度表达对TORC1的急性过度激活通过募集AMPA受体促进兴奋性突触的成熟。有趣的是，TORC1 过度激活不影响抑制性传递，导致兴奋性与抑制性比率的显着失衡。Rheb 过度表达还扩大了 tectal 神经元中的兴奋性视觉输入场，这与视网膜输入细化和细胞整合到电路中的失调一致。与其他主要发现使用 TORC1 调节蛋白的广泛系统性缺失或突变导致突触抑制受损的报告相比，我们从急性、