Mutafova-Yambolieva Violeta N, Durnin Leonie
Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Pharmacol Ther. 2014 Nov;144(2):162-91. doi: 10.1016/j.pharmthera.2014.05.012. Epub 2014 Jun 2.
The past half century has witnessed tremendous advances in our understanding of extracellular purinergic signaling pathways. Purinergic neurotransmission, in particular, has emerged as a key contributor in the efficient control mechanisms in the nervous system. The identity of the purine neurotransmitter, however, remains controversial. Identifying it is difficult because purines are present in all cell types, have a large variety of cell sources, and are released via numerous pathways. Moreover, studies on purinergic neurotransmission have relied heavily on indirect measurements of integrated postjunctional responses that do not provide direct information for neurotransmitter identity. This paper discusses experimental support for adenosine 5'-triphosphate (ATP) as a neurotransmitter and recent evidence for possible contribution of other purines, in addition to or instead of ATP, in chemical neurotransmission in the peripheral, enteric and central nervous systems. Sites of release and action of purines in model systems such as vas deferens, blood vessels, urinary bladder and chromaffin cells are discussed. This is preceded by a brief discussion of studies demonstrating storage of purines in synaptic vesicles. We examine recent evidence for cell type targets (e.g., smooth muscle cells, interstitial cells, neurons and glia) for purine neurotransmitters in different systems. This is followed by brief discussion of mechanisms of terminating the action of purine neurotransmitters, including extracellular nucleotide hydrolysis and possible salvage and reuptake in the cell. The significance of direct neurotransmitter release measurements is highlighted. Possibilities for involvement of multiple purines (e.g., ATP, ADP, NAD(+), ADP-ribose, adenosine, and diadenosine polyphosphates) in neurotransmission are considered throughout.
在过去的半个世纪里,我们对细胞外嘌呤能信号通路的理解取得了巨大进展。特别是嘌呤能神经传递已成为神经系统高效控制机制的关键因素。然而,嘌呤神经递质的身份仍存在争议。识别它很困难,因为嘌呤存在于所有细胞类型中,有多种细胞来源,并通过多种途径释放。此外,对嘌呤能神经传递的研究严重依赖于对整合的节后反应的间接测量,而这些测量并不能提供神经递质身份的直接信息。本文讨论了支持三磷酸腺苷(ATP)作为神经递质的实验证据,以及除ATP之外或替代ATP的其他嘌呤在周围、肠和中枢神经系统化学神经传递中可能发挥作用的最新证据。还讨论了嘌呤在诸如输精管、血管、膀胱和嗜铬细胞等模型系统中的释放和作用位点。在此之前,先简要讨论了证明嘌呤储存在突触小泡中的研究。我们研究了不同系统中嘌呤神经递质的细胞类型靶点(如平滑肌细胞、间质细胞、神经元和神经胶质细胞)的最新证据。随后简要讨论了终止嘌呤神经递质作用的机制,包括细胞外核苷酸水解以及细胞内可能的补救和再摄取。强调了直接测量神经递质释放的重要性。文中还探讨了多种嘌呤(如ATP、ADP、NAD(+)、ADP - 核糖、腺苷和二腺苷多磷酸)参与神经传递的可能性。