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嘌呤核苷对成人大脑神经可塑性的影响。

The impact of purine nucleosides on neuroplasticity in the adult brain.

作者信息

Dos Santos Beatriz, Piermartiri Tetsade, Tasca Carla I

机构信息

Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, 88040-900, Brazil.

Programa de Pós-Graduação Em Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.

出版信息

Purinergic Signal. 2025 Feb;21(1):113-131. doi: 10.1007/s11302-024-09988-9. Epub 2024 Feb 17.

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应对内部和外部刺激时,调整和重组其细胞结构及神经网络的能力。在成年人中,这一过程涉及神经发生、突触形成以及突触和神经化学可塑性。多项研究报告了嘌呤能系统对神经可塑性调节的重大影响。而且,有大量证据支持嘌呤核苷,如腺苷、肌苷和鸟苷,在这一过程中的作用。本综述展示了关于这些核苷如何增强成体中枢神经系统神经可塑性,尤其是在应对损伤时的广泛研究。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,特别是A1R和A2AR的相互作用。A1R的激活似乎会抑制神经元分化并促进星形胶质细胞生成,而A2AR的激活则支持神经发生、神经突生长和突触可塑性。肌苷和鸟苷对细胞增殖、神经发生和神经突生长有积极影响。肌苷似乎能调节细胞外腺苷水平,而鸟苷可能通过嘌呤能系统和谷氨酸能系统之间的相互作用发挥作用。此外,该综述还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,强调了这些核苷在脑功能神经可塑性和恢复中的重要性。

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