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Less neurogenesis and inflammation in the immature than in the juvenile brain after cerebral hypoxia-ischemia

Journal article
Authors L. Qiu
Changlian Zhu
Xiaoyang Wang
F. Xu
Peter S Eriksson
Michael Nilsson
Christiana M Cooper-Kuhn
Hans-Georg Kuhn
Klas Blomgren
Published in J Cereb Blood Flow Metab
Volume 27
Issue 4
Pages 785-94
ISSN 0271-678X (Print)
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences
Pages 785-94
Language en
Links dx.doi.org/10.1038/sj.jcbfm.9600385
Keywords Aging/*pathology, Animals, Antimetabolites/diagnostic use, Bromodeoxyuridine/diagnostic use, Cell Count, Cell Differentiation/drug effects, Cell Proliferation, Dentate Gyrus/pathology, Hippocampus/pathology, Hypoxia-Ischemia, Brain/*pathology, Immunohistochemistry, Inflammation/*pathology, Male, Mice, Mice, Inbred C57BL, Nerve Tissue Proteins/genetics, Neuroglia/pathology, Neurons/*pathology, Nuclear Proteins/genetics
Subject categories Neuroscience, Experimental brain research, Molecular neurobiology, Neurobiology

Abstract

The effects of hypoxia-ischemia (HI) on proliferation and differentiation in the immature (postnatal day 9) and juvenile (postnatal day 21) mouse hippocampus were investigated by injecting bromodeoxyuridine (50 mg/kg) daily for 7 days after the insult and evaluating the labeling 5 weeks after HI. Phenotypic differentiation was evaluated using NeuN, Iba1, APC, and S100beta as markers of neurons, microglia, oligodendrocytes, and astrocytes, respectively. The basal proliferation, in particular neurogenesis, was higher in the immature than in the juvenile hippocampus. Hypoxia-ischemia did not increase neurogenesis significantly in the immature dentate gyrus (DG), but it increased several-fold in the juvenile brain, reaching the same level as in the normal, noninjured immature brain. This suggests that the immature hippocampus is already working at the top of its proliferative capacity and that even though basal neurogenesis decreased with age, the injury-induced generation of new neurons in the juvenile hippocampus could not increase beyond the basal level of the immature brain. Generation of glial cells of all three types after HI was significantly more pronounced in the cornu ammonis of the hippocampus region of the juvenile hippocampus. In the DG, only microglia production was greater in the juvenile brain. Increased microglia proliferation correlated with increased levels of the proinflammatory cytokines MCP-1 and IL-18 3 days after HI, indicating that the inflammatory response is stronger in the juvenile hippocampus. In summary, contrary to what has been generally assumed, our results indicate that the juvenile brain has a greater capacity for neurogenesis after injury than the immature brain.

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