scholarly journals Ion Channels and Zinc: Mechanisms of Neurotoxicity and Neurodegeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Deborah R. Morris ◽  
Cathy W. Levenson

Ionotropic glutamate receptors, such as NMDA, AMPA and kainate receptors, are ligand-gated ion channels that mediate much of the excitatory neurotransmission in the brain. Not only do these receptors bind glutamate, but they are also regulated by and facilitate the postsynaptic uptake of the trace metal zinc. This paper discusses the role of the excitotoxic influx and accumulation of zinc, the mechanisms responsible for its cytotoxicity, and a number of disorders of the central nervous system that have been linked to these neuronal ion channels and zinc toxicity including ischemic brain injury, traumatic brain injury, and epilepsy.

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
So Yeong Cheon ◽  
Eun Jung Kim ◽  
Jeong Min Kim ◽  
Bon-Nyeo Koo

Stroke has become a more common disease worldwide. Despite great efforts to develop treatment, little is known about ischemic stroke. Cerebral ischemia activates multiple cascades of cell type-specific pathomechanisms. Ischemic brain injury consists of a complex series of cellular reactions in various cell types within the central nervous system (CNS) including platelets, endothelial cells, astrocytes, neutrophils, microglia/macrophages, and neurons. Diverse cellular changes after ischemic injury are likely to induce cell death and tissue damage in the brain. Since cells in the brain exhibit different functional roles at distinct time points after injury (acute/subacute/chronic phases), it is difficult to pinpoint genuine roles of cell types after brain injury. Many experimental studies have shown the association of apoptosis signal-regulating kinase 1 (ASK1) with cellular pathomechanisms after cerebral ischemia. Blockade of ASK1, by either pharmacological or genetic manipulation, leads to reduced ischemic brain injury and subsequent neuroprotective effects. In this review, we present the cell type-specific pathophysiology of the early phase of ischemic stroke, the role of ASK1 suggested by preclinical studies, and the potential use of ASK suppression, either by pharmacologic or genetic suppression, as a promising therapeutic option for ischemic stroke recovery.


2017 ◽  
Vol 14 (4) ◽  
pp. 2937-2942 ◽  
Author(s):  
Lixiao Pan ◽  
Fengyun Yang ◽  
Caixia Lu ◽  
Changxin Jia ◽  
Qing Wang ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 8 (4) ◽  
pp. 5670-5671
Author(s):  
Zhifeng Qi ◽  
Ke Jian Liu

2012 ◽  
pp. 9-17
Author(s):  
Bentham Science Publisher Bentham Science Publisher

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