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Sublethal Transient Global Ischemia Stimulates Migration of Neuroblasts and Neurogenesis in Mice

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Translational Stroke Research : Volume 1, Issue 2, June 2010

Translational Stroke Research : Volume 1, Issue 1, March 2010

Sublethal Transient Global Ischemia Stimulates Migration of Neuroblasts and Neurogenesis in Mice

Content Provider	Springer Nature Link
Author	Li, Ying Yu, Shan Ping Mohamad, Osama Genetta, Thomas Wei, Ling
Copyright Year	2010
Abstract	Increasing evidence has shown the potential of neuronal plasticity in adult brain after injury. Neural proliferation can be triggered by a focal sublethal ischemic preconditioning event; whether mild global ischemia could cause neurogenesis has been not clear. The present study investigated stimulating effects of sublethal transient global ischemia (TGI) on endogenous neurogenesis and neuroblast migration in the subventricular zone (SVZ), dentate gyrus, and peri-infarct areas of the adult cortex. Adult mice of 129S2/Sv strain were subjected to 8-min bilateral common carotid artery ligation followed by 5-bromo-2′-deoxyuridine (BrdU; 50 mg/kg, intraperitoneal) administration every day until being sacrificed at 1–21 days after reperfusion. The mild TGI did not induce neuronal cell death for up to 7 days after TGI, as evidenced by negative terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining among NeuN-positive cells in the hippocampus and neocortex. In TGI animals, BrdU staining revealed enhanced proliferation of neuroblasts and their migration track from the SVZ into the striatum and neocortex. In the corpus callosum, there were more BrdU-positive cells in the TGI group in the first 2 days. Increasing numbers of BrdU-positive cells were seen 7–21 days later in the striatum and cortex of TGI mice. The cortex of TGI animals showed increased expression of erythropoietin, erythropoietin receptor, fibroblast growth factor 2, vascular endothelial growth factor, and phosphorylated Jun N-terminal kinase; the expression was peaked 2 to 3 days after reperfusion. BrdU and NeuN double staining in the dentate gyrus, striatum, and cortex implied increased neurogenesis induced by the TGI preconditioning. Doublecortin (DCX)-positive cells increased in the cortex of TGI mice, localized to cortical layers II, III, and V, and many stained positive for the mature neuronal markers NeuN, neurofilament, N-methyl-d-aspartic acid receptor subunit gene NR1, or the gamma-aminobutyric-acid-synthesizing enzyme glutamic acid decarboxylase (GAD67). The atypical localization of DCX-positive cells and the colabeling with mature neuronal markers suggested that, in addition to indentifying migrating neuroblasts, DCX might also be a stress marker in the cortex. It is suggested that the sublethal TGI-induced regenerative responses may contribute to the beneficial effects of ischemic preconditioning.
Starting Page	184
Ending Page	196
Page Count	13
File Format	PDF
ISSN	18684483
Journal	Translational Stroke Research
Volume Number	1
Issue Number	3
e-ISSN	1868601X
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-03-30
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Transient global ischemia Neuroblasts Neurogenesis Cell migration Doublecortin (DCX) Subventricular zone (SVZ) Vascular Surgery Neurosurgery Cardiology Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Neurology (clinical)

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