Zinc in the central nervous system: From molecules to behavior

被引:149
|
作者
Gower-Winter, Shannon D. [1 ]
Levenson, Cathy W. [1 ,2 ]
机构
[1] Florida State Univ, Dept Biomed Sci, Coll Med, Tallahassee, FL 32306 USA
[2] Florida State Univ, Coll Med, Program Neurosci, Tallahassee, FL 32306 USA
关键词
zinc; brain; zinc finger; neurogenesis; neurotoxicity; Alzheimer's disease; depression; traumatic brain injury; stroke; seizure; TRAUMATIC BRAIN-INJURY; ALZHEIMERS-DISEASE; ADULT RATS; HIPPOCAMPAL-NEURONS; MAJOR DEPRESSION; DEFICIENT DIET; UNITED-STATES; SYNAPTIC ZINC; SERUM ZINC; MICE;
D O I
10.1002/biof.1012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The trace metal zinc is a biofactor that plays essential roles in the central nervous system across the lifespan from early neonatal brain development through the maintenance of brain function in adults. At the molecular level, zinc regulates gene expression through transcription factor activity and is responsible for the activity of dozens of key enzymes in neuronal metabolism. At the cellular level, zinc is a modulator of synaptic activity and neuronal plasticity in both development and adulthood. Given these key roles, it is not surprising that alterations in brain zinc status have been implicated in a wide array of neurological disorders including impaired brain development, neurodegenerative disorders such as Alzheimer's disease, and mood disorders including depression. Zinc has also been implicated in neuronal damage associated with traumatic brain injury, stroke, and seizure. Understanding the mechanisms that control brain zinc homeostasis is thus critical to the development of preventive and treatment strategies for these and other neurological disorders.
引用
收藏
页码:186 / 193
页数:8
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