Extracellular vesicles (EVs) play an important role in intercellular communication as carriers of signalling molecules such as bioactive miRNAs, proteins and lipids. EVs are key players in the functioning of the central nervous system (CNS) by influencing synaptic events and modulating recipient neurons. However, the specific role of neuron-to-neuron communication via EVs is still not well understood. Here, we provide evidence that primary neurons uptake neuron-derived EVs in the soma, dendrites, and even in the dendritic spines, and carry synaptic proteins. Neuron-derived EVs increased spine density and promoted the phosphorylation of Akt and ribosomal protein S6 (RPS6), via TrkB-signalling, without impairing the neuronal network activity. Strikingly, EVs exerted a trophic effect on challenged nutrient-deprived neurons. Altogether, our results place EVs in the spotlight for synaptic plasticity modulation as well as a possible therapeutic tool to fight neurodegeneration.

中文翻译：

---

神经元衍生的细胞外囊泡含有突触蛋白，促进脊柱形成，激活 TrkB 介导的信号传导并保持神经元复杂性

细胞外囊泡 (EV) 作为生物活性 miRNA、蛋白质和脂质等信号分子的载体，在细胞间通讯中发挥着重要作用。EV 通过影响突触事件和调节受体神经元，在中枢神经系统 (CNS) 功能中发挥关键作用。然而，通过电动汽车进行神经元间通信的具体作用仍不清楚。在这里，我们提供的证据表明，初级神经元在体细胞、树突甚至树突棘中摄取神经元衍生的 EV，并携带突触蛋白。神经元衍生的 EV 通过 TrkB 信号传导增加脊柱密度并促进 Akt 和核糖体蛋白 S6 (RPS6) 的磷酸化，而不会损害神经元网络活动。引人注目的是，EV 对受到营养缺乏的神经元产生了营养作用。总而言之，我们的结果使电动汽车成为突触可塑性调节的焦点，并成为对抗神经退行性变的可能的治疗工具。