Insight into Glutamate Excitotoxicity from Synaptic Zinc Homeostasis

• Published in: International journal of alzheimer's disease Vol. 2011; no. 2011; pp. 1 - 8
• Main Author: Takeda, Atsushi
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Puplishing Corporation 2011; SAGE-Hindawi Access to Research; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: Alzheimer's disease; Development and progression; Glutamate; Neurons; Physiological aspects; Review; Zinc in the body; Japan
• ISSN: 2090-8024; 2090-0252; 2090-0252
• DOI: 10.4061/2011/491597

Zinc is released from glutamatergic (zincergic) neuron terminals in the hippocampus, followed by the increase in Zn2+ concentration in the intracellular (cytosol) compartment, as well as that in the extracellular compartment. The increase in Zn2+ concentration in the intracellular compartment during synaptic excitation is mainly due to Zn2+ influx through calcium-permeable channels and serves as Zn2+ signaling as well as the case in the extracellular compartment. Synaptic Zn2+ homeostasis is important for glutamate signaling and altered under numerous pathological processes such as Alzheimer's disease. Synaptic Zn2+ homeostasis might be altered in old age, and this alteration might be involved in the pathogenesis and progression of Alzheimer's disease; Zinc may play as a key-mediating factor in the pathophysiology of Alzheimer's disease. This paper summarizes the role of Zn2+ signaling in glutamate excitotoxicity, which is involved in Alzheimer's disease, to understand the significance of synaptic Zn2+ homeostasis in the pathophysiology of Alzheimer's disease.