Laboratory of Molecular and Cellular Pharmacology of Purinergic Transmission, Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133, Milano, Italy,
Purinergic Signal. 2006 Nov;2(4):595-604. doi: 10.1007/s11302-006-9016-0. Epub 2006 Jun 20.
Central nervous system glial cells release and respond to nucleotides under both physiological and pathological conditions, suggesting that these molecules play key roles in both normal brain function and in repair after damage. In particular, ATP released from astrocytes activates P2 receptors on astrocytes and other brain cells, allowing a form of homotypic and heterotypic signalling, which also involves microglia, neurons and oligodendrocytes. Multiple P2X and P2Y receptors are expressed by both astrocytes and microglia; however, these receptors are differentially recruited by nucleotides, depending upon specific pathophysiological conditions, and also mediate the long-term trophic changes of these cells during inflammatory gliosis. In astrocytes, P2-receptor-induced gliosis occurs via activation of the extracellular-regulated kinases (ERK) and protein kinase B/Akt pathways and involves induction of inflammatory and anti-inflammatory genes, cyclins, adhesion and antiapoptotic molecules. While astrocytic P2Y₁ and P2Y(₂,₄) are primarily involved in short-term calcium-dependent signalling, multiple P2 receptor subtypes seem to cooperate to astrocytic long-term changes. Conversely, in microglia, exposure to inflammatory and immunological stimuli results in differential functional changes of distinct P2 receptors, suggesting highly specific roles in acquisition of the activated phenotype. We believe that nucleotide-induced activation of astrocytes and microglia may originally start as a defence mechanism to protect neurons from cytotoxic and ischaemic insults; dysregulation of this process in chronic inflammatory diseases eventually results in neuronal cell damage and loss. On this basis, full elucidation of the specific roles of P2 receptors in these cells may help exploit the beneficial neuroprotective features of activated glia while attenuating their harmful properties and thus provide the basis for novel neuroprotective strategies that specifically target the purinergic system.
中枢神经系统胶质细胞在生理和病理条件下释放和响应核苷酸,表明这些分子在正常大脑功能和损伤后修复中发挥关键作用。特别是,星形胶质细胞释放的 ATP 激活星形胶质细胞和其他脑细胞上的 P2 受体,允许同种型和异型信号传递,其中还涉及小胶质细胞、神经元和少突胶质细胞。星形胶质细胞和小胶质细胞均表达多种 P2X 和 P2Y 受体;然而,这些受体根据特定的病理生理条件被不同的核苷酸募集,并且还介导这些细胞在炎症性神经胶质增生过程中的长期营养变化。在星形胶质细胞中,P2 受体诱导的神经胶质增生通过细胞外调节激酶 (ERK) 和蛋白激酶 B/Akt 途径的激活发生,并涉及炎症和抗炎基因、细胞周期蛋白、黏附分子和抗凋亡分子的诱导。虽然星形胶质细胞 P2Y₁ 和 P2Y(₂,₄) 主要参与短期钙依赖性信号传递,但多种 P2 受体亚型似乎合作以实现星形胶质细胞的长期变化。相反,在小胶质细胞中,暴露于炎症和免疫刺激会导致不同 P2 受体的功能变化,这表明在获得激活表型方面具有高度特异性作用。我们认为,核苷酸诱导的星形胶质细胞和小胶质细胞的激活最初可能是一种保护神经元免受细胞毒性和缺血性损伤的防御机制;在慢性炎症性疾病中,这种过程的失调最终导致神经元细胞损伤和丧失。在此基础上,充分阐明 P2 受体在这些细胞中的特定作用可能有助于利用激活的胶质细胞的有益神经保护特性,同时减轻其有害特性,从而为专门针对嘌呤能系统的新型神经保护策略提供基础。