This study aimed to investigate the effect of the neuregulin-1/epidermal growth factor 4 (NRG1/ErbB4) signaling pathway on visual cortex synaptic plasticity in adult amblyopic rats with monocular deprivation (MD). Compared with the control group, the P wave latency and amplitude of the MD group were prolonged and low, respectively, with reduced synaptic plasticity-related protein expression, lower number of visual cortex neurons, and increased apoptosis of visual cortex neurons. Recombinant neuregulin-1 (rNRG1) administration activated the NRG1/ErbB4 signaling pathway and improved the visual cortex synaptic plasticity in MD amblyopic rats. However, the effects of rNRG1 were reversed by AG1478 (ErbB4 receptor blockers). The NRG1/ErbB4 signaling pathway in the parvalbumin neurons from MD rats was also inactivated. Amblyopic rats had significantly low cell activity and downregulated expression of synaptic plasticity-related proteins. Thus, exogenous administration of NRG1 can activate ErbB4 signal transduction and improve the damaged synaptic plasticity of the visual cortex among amblyopic rats. Further studies are warranted to explore the potential for clinical management of amblyopia.

中文翻译：

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NRG1/ErbB4信号通路调控对弱视成年大鼠视皮层突触可塑性的影响

本研究旨在探讨神经调节蛋白-1/表皮生长因子 4 (NRG1/ErbB4) 信号通路对单眼剥夺 (MD) 成年弱视大鼠视觉皮层突触可塑性的影响。与对照组相比，MD组的P波潜伏期和幅度分别延长和降低，突触可塑性相关蛋白表达减少，视觉皮层神经元数量减少，视觉皮层神经元凋亡增加。重组神经调节蛋白-1 (rNRG1) 给药激活了 NRG1/ErbB4 信号通路并改善了 MD 弱视大鼠的视觉皮层突触可塑性。然而，rNRG1 的作用被 AG1478（ErbB4 受体阻滞剂）逆转。MD 大鼠小清蛋白神经元中的 NRG1/ErbB4 信号通路也被灭活。弱视大鼠的细胞活性显着降低，突触可塑性相关蛋白的表达下调。因此，外源性给予NRG1可以激活ErbB4信号转导，改善弱视大鼠视皮层受损的突触可塑性。需要进一步的研究来探索弱视临床管理的潜力。