摘要
ATP在中枢神经系统(CNS)中的有效作用在20世纪40年代已被报道;嘌呤和嘧啶受体的克隆与特征,直到90年代初才被报道。它确定了七个P2X离子通道受体亚型,其中三个以同源多聚体或杂多聚体形成阳离子通道。P2X受体亚型广泛表达于中枢神经系统,它们的分布被不同的领域报道。它们在突触传递和神经调节,以及在营养信号方面发挥作用。从神经和星形胶质细胞释放的 ATP主要参与神经元 - 神经胶质相互作用。嘌呤信号参与正常的行为,包括学习和记忆,睡眠和觉醒,运动和摄食活动和认知。P2X受体参与CNS的病理生理学,包括外伤、炎症、阿尔茨海默氏症和帕金森氏病、多发性硬化和肌萎缩性侧索硬化症、抑郁和焦虑。P2X4和P2X7受体拮抗剂是通过小神经胶质细胞对神经性疼痛发挥治疗作用,而P2X3受体拮抗剂也减轻神经性疼痛,只是通过不同的机制。
关键词: ATP ,脑干,胶质,谷氨酸,海马,存储器,神经变性疾病,神经性疼痛,神经保护,脊髓。
Current Medicinal Chemistry
Title:Physiopathological Roles of P2X Receptors in the Central Nervous System
Volume: 22 Issue: 7
Author(s): G. Burnstock
Affiliation:
关键词: ATP ,脑干,胶质,谷氨酸,海马,存储器,神经变性疾病,神经性疼痛,神经保护,脊髓。
摘要: Potent actions of ATP in the central nervous system (CNS) were reported in the late 1940’s, but cloning and characterisation of receptors for purines and pyrimidines did not take place until the early 1990’s, which identified seven P2X ion channel receptor subtypes, three of which form the cation channel as homomultimers or heteromultimers. P2X receptor subtypes are widely expressed in the CNS and their distribution is described in different regions. They function in synaptic cotransmission and neuromodulation, as well as in trophic signalling. ATP released from nerves and astroglial cells are predominantly involved in neuron-glial interactions. Purinergic signalling is involved in normal behaviour, including learning and memory, sleep and arousal, locomotor and feeding activities and cognition. P2X receptors participate in CNS pathophysiology, including injury, inflammation, Alzheimer’s and Parkinson’s diseases, multiple sclerosis and amyotrophic lateral sclerosis, depression and anxiety. P2X4 and P2X7 receptor antagonists are effective via microglia against neuropathic pain, while P2X3 receptor antagonists also reduce neuropathic pain, but via a differernt mechanism.
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Cite this article as:
G. Burnstock , Physiopathological Roles of P2X Receptors in the Central Nervous System, Current Medicinal Chemistry 2015; 22 (7) . https://dx.doi.org/10.2174/0929867321666140706130415
DOI https://dx.doi.org/10.2174/0929867321666140706130415 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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