Abstract：
Neuroplasticity refers to the nervous system\'s ability to adapt and reorganize its cell structures and neuronal networks in response to internal and external stimuli. In adults, this process involves neurogenesis, synaptogenesis, and synaptic and neurochemical plasticity. Several studies have reported the significant impact of the purinergic system on neuroplasticity modulation. And, there is considerable evidence supporting the role of purine nucleosides, such as adenosine, inosine, and guanosine, in this process. This review presents extensive research on how these nucleosides enhance the neuroplasticity of the adult central nervous system, particularly in response to damage. The mechanisms through which these nucleosides exert their effects involve complex interactions with various receptors and signaling pathways. Adenosine\'s influence on neurogenesis involves interactions with adenosine receptors, specifically A1R and A2AR. A1R activation appears to inhibit neuronal differentiation and promote astrogliogenesis, while A2AR activation supports neurogenesis, neuritogenesis, and synaptic plasticity. Inosine and guanosine positively impact cell proliferation, neurogenesis, and neuritogenesis. Inosine seems to modulate extracellular adenosine levels, and guanosine might act through interactions between purinergic and glutamatergic systems. Additionally, the review discusses the potential therapeutic implications of purinergic signaling in neurodegenerative and neuropsychiatric diseases, emphasizing the importance of these nucleosides in the neuroplasticity of brain function and recovery.
摘要：
神经可塑性是指神经系统在响应内部和外部刺激时适应和重组其细胞结构和神经元网络的能力。在成年人中,这个过程涉及神经发生，突触发生,突触和神经化学可塑性。一些研究已经报道了嘌呤能系统对神经可塑性调节的显著影响。And,有大量证据支持嘌呤核苷的作用，如腺苷，肌苷,和鸟苷,在这个过程中。这篇综述对这些核苷如何增强成人中枢神经系统的神经可塑性进行了广泛的研究。特别是对损坏的反应。这些核苷发挥作用的机制涉及与各种受体和信号通路的复杂相互作用。腺苷对神经发生的影响涉及与腺苷受体的相互作用，特别是A1R和A2AR。A1R激活似乎抑制神经元分化并促进星形胶质细胞生成，虽然A2AR激活支持神经发生，神经发生，和突触可塑性。肌苷和鸟苷积极影响细胞增殖，神经发生，和神经生成。肌苷似乎调节细胞外腺苷水平，鸟苷可能通过嘌呤能和谷氨酸能系统之间的相互作用起作用。此外,这篇综述讨论了嘌呤能信号在神经退行性疾病和神经精神疾病中的潜在治疗意义，强调这些核苷在脑功能和恢复的神经可塑性中的重要性。
