Relationship between Zinc (Zn (2+) ) and Glutamate Receptors in the Processes Underlying Neurodegeneration.
Relationship between Zinc (Zn (2+) ) and Glutamate Receptors in the Processes Underlying Neurodegeneration.
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DOI：
10.1155/2015/591563
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发表时间：
2015
影响因子：
3.1
通讯作者：
Szewczyk B
中科院分区：
文献类型：
--
作者：
Pochwat B;Nowak G;Szewczyk B
大量研究结果表明，特定神经递质之间的失衡可能会导致大脑回路功能障碍和许多病理状态的发展。谷氨酸通路对神经系统功能的意义是模棱两可的。一方面，谷氨酸传递是神经可塑性、突触发生或细胞生存所必需的，但另一方面，突触中谷氨酸水平的过度和持续增加可能导致细胞死亡。在临床情况下，谷氨酸系统的过度活跃与缺血、癫痫和神经退行性疾病如阿尔茨海默氏症、亨廷顿氏症和许多其他疾病有关。谷氨酸活性在生理范围内的实现需要内源调节因子的有效调控。由于锌离子游离池是一些谷氨酸神经元中的一种共递质，这一元素在神经退行性疾病的病理生理学中的作用已被深入研究。有大量证据表明，在缺血性和神经退行性疾病中存在锌离子代谢紊乱和谷氨酸系统的异常。然而，锌离子调控功能与谷氨酸系统之间的确切相互作用仍不完全清楚。本文综述了在特定的病理中枢神经系统(CNS)条件下，锌离子与谷氨酸依赖的信号通路之间的关系。
The results from numerous studies have shown that an imbalance between particular neurotransmitters may lead to brain circuit dysfunction and development of many pathological states. The significance of glutamate pathways for the functioning of the nervous system is equivocal. On the one hand, glutamate transmission is necessary for neuroplasticity, synaptogenesis, or cell survival, but on the other hand an excessive and long-lasting increased level of glutamate in the synapse may lead to cell death. Under clinical conditions, hyperactivity of the glutamate system is associated with ischemia, epilepsy, and neurodegenerative diseases such as Alzheimer's, Huntington's, and many others. The achievement of glutamate activity in the physiological range requires efficient control by endogenous regulatory factors. Due to the fact that the free pool of ion Zn2+ is a cotransmitter in some glutamate neurons; the role of this element in the pathophysiology of a neurodegenerative diseases has been intensively studied. There is a lot of evidence for Zn2+ dyshomeostasis and glutamate system abnormalities in ischemic and neurodegenerative disorders. However, the precise interaction between Zn2+ regulative function and the glutamate system is still not fully understood. This review describes the relationship between Zn2+ and glutamate dependent signaling pathways under selected pathological central nervous system (CNS) conditions.
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影响因子：
15.1
作者：
Bjorklund NL;Reese LC;Sadagoparamanujam VM;Ghirardi V;Woltjer RL;Taglialatela G
通讯作者：
Taglialatela G
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5.7
作者：
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