Review

Role of astrocytes in manganese mediated neurotoxicity

Marta Sidoryk-Wegrzynowicz¹ and Michael Aschner^12*

• * Corresponding author: Michael Aschner michael.aschner@vanderbilt.edu

Author Affiliations

¹ Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 23233, USA

² Department of Pharmacology, the Kennedy Center for Research on Human Development, and the Center for Molecular Toxicology, Vanderbilt University Medical Center, Nashville, TN 23233, USA

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BMC Pharmacology and Toxicology 2013, 14:23 doi:10.1186/2050-6511-14-23

Published: 18 April 2013

Abstract

Astrocytes are responsible for numerous aspects of metabolic support, nutrition, control of the ion and neurotransmitter environment in central nervous system (CNS). Failure by astrocytes to support essential neuronal metabolic requirements plays a fundamental role in the pathogenesis of brain injury and the ensuing neuronal death. Astrocyte-neuron interactions play a central role in brain homeostasis, in particular via neurotransmitter recycling functions. Disruption of the glutamine (Gln)/glutamate (Glu) -γ-aminobutyric acid (GABA) cycle (GGC) between astrocytes and neurons contributes to changes in Glu-ergic and/or GABA-ergic transmission, and is associated with several neuropathological conditions, including manganese (Mn) toxicity. In this review, we discuss recent advances in support of the important roles for astrocytes in normal as well as neuropathological conditions primarily those caused by exposure to Mn.