Zinc inhibits astrocyte glutamate uptake by activation of poly(ADP-ribose) polymerase-1

Suh, SW; Aoyama, K; Alano, CC; Anderson, CM; Hamby, AM; Swanson, RA

HERO ID

525496

Reference Type

Journal Article

Year

2007

Language

English

PMID

17728843

HERO ID 525496
In Press No
Year 2007
Title Zinc inhibits astrocyte glutamate uptake by activation of poly(ADP-ribose) polymerase-1
Authors Suh, SW; Aoyama, K; Alano, CC; Anderson, CM; Hamby, AM; Swanson, RA
Journal Molecular Medicine
Volume 13
Issue 7-8
Page Numbers 344-349
Abstract Several processes by which astrocytes protect neurons during ischemia are now well established. However, less is known about how neurons themselves may influence these processes. Neurons release zinc (Zn2+)from presynaptic terminals during ischemia, seizure, head trauma, and hypoglycemia, and modulate postsynaptic neuronal function. Peak extracellular zinc may reach concentrations as high as 400 mu M. Excessive levels of free, ionic zinc can initiate DNA damage and the subsequent activation of poly(ADP-ribose) polymerase I (PARP-1), which in turn lead to NAD(+) and ATP depletion when DNA damage is extensive. In this study, cultured cortical astrocytes were used to explore the effects of zinc on astrocyte glutamate uptake, an energy-dependent process that is critical for neuron survival, Astrocytes incubated with 100 or 400 mu M of zinc for 30 min showed significant decreases in ATP levels and glutamate uptake capacity. These changes were prevented by the PARP inhibitors benzamide or DPQ (3,4-dihydro-5-(4-(1-piperidinyl)butoxyl)-1 (2H-isoquinolinone) or PARP-1 gene deletion (PARP-1 KO). These findings suggest that release of Zn2+ from neurons during brain insults could induce PARP-1 activation in astrocytes, leading to impaired glutamate uptake and exacerbation of neuronal injury.
Doi 10.2119/2007-00043.Suh
Pmid 17728843
Wosid WOS:000249050300004
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword focal cerebral-ischemia; traumatic brain-injury; cell-death; neuronal; death; nitric-oxide; dna-damage; intracellular zinc; adp-ribosylation; cortical-neurons; nervous-system
Is Qa No