Zinc homeostasis and brain injury

Stefano Sensi; Erica Rockabrand; Israel Sekler

doi:10.1007/978-0-387-70830-0_10

Zinc homeostasis and brain injury

Stefano Sensi, Erica Rockabrand, Israel Sekler

Physiology and Cell Biology

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

1 Scopus citations

Abstract

Cumulating evidence suggest that Zn2+ dys/homeostasis can play a major role in promoting brain injury in excitotoxic syndromes. Zn2+ homeostasis in the brain is regulated through highly dynamic pathways and is deeply connected with other major signaling pathways, such as NO- and MAP kinase-dependent systems. Zn2+ signaling in neurons and glia also interplays with proton and Ca2+ homeostasis. Zn2+ appears to promote injury with greater potency compared to Ca2+ and as such the cation may be an underappreciated mediator of excitotoxicity, which for many years has been described mainly as a Ca2+- dependent phenomenon.

Original language	English
Title of host publication	Interaction Between Neurons and Glia in Aging and Disease
Publisher	Springer US
Pages	221-244
Number of pages	24
ISBN (Print)	9780387708294
DOIs	https://doi.org/10.1007/978-0-387-70830-0_10
State	Published - 1 Dec 2007

ASJC Scopus subject areas

General Neuroscience

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BT - Interaction Between Neurons and Glia in Aging and Disease

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Zinc homeostasis and brain injury

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