Zinc in the central nervous system: From molecules to behavior

Abstract

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.

The effects of interactions between selenium and zinc serum concentration and SEP15 and SLC30A3 gene polymorphisms on memory scores in a population of mature and elderly adults

“…The ZnT3 protein (encoded by the SLC30A3 gene) belongs to a class of proteins whose function is to lower the intracellular zinc concentrations, facilitating efflux of intracellular vesicles in the cytoplasm and/or extracellular spaces, and plays a particularly important role in neuronal zinc regulation. This protein is responsible for the accumulation of free zinc in glutamatecontaining vesicles found in the hippocampus and cortex (Gower-Winte and Levenson 2012). The SLC30A3 gene is expressed in brain regions important for cognitive development and development of different kinds of memory, such as the hippocampus, cerebral cortex, and amygdale (Seve et al 2004), and ZnT3 knock-out mice exhibit cognitive loss, alterations in memory and may represent a phenocopy for memory deficits of Alzheimer's disease (Adlard et al 2010;Martel et al 2010;.…”

Zinc in traumatic brain injury

“…An abundance of previous work has shown that free zinc, sequestered in synaptic vesicles, is released from neurons into the synaptic cleft where it results in postsynaptic neuronal death [2]. Although the release of synaptic zinc after injury is well accepted in the field, there have been indicators that other pools of free zinc may contribute to neuronal damage after injury.…”

“…The essential trace element zinc has been implicated in many disorders of the central nervous system such as TBI, ischemia, stroke, and mood disorders including depression [2].…”

Mapping the dynamics of cortical neuroplasticity of skilled motor learning using micro X-ray fluorescence and histofluorescence imaging of zinc in the rat

“…Zn also regulates expression of immediate early genes (e.g. c-Fos) in response to brain and behavioral activity through zinc finger transcription factors [18]. Abnormally low amounts of Zn in the brain can also induce learning and memory deficits, although results are not consistent.…”