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Age-dependent regenerative responses in the striatum and cortex after hypoxia-ischemia.

Artikel i vetenskaplig tidskrift
Författare Changlian Zhu
Lin Qiu
Xiaoyang Wang
Falin Xu
Michael Nilsson
Christiana M Cooper-Kuhn
Hans-Georg Kuhn
Klas Blomgren
Publicerad i Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
Volym 29
Nummer/häfte 2
Sidor 342-54
ISSN 1559-7016
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 342-54
Språk en
Länkar dx.doi.org/10.1038/jcbfm.2008.124
Ämnesord gliogenesis, inflammation, juvenile brain, neonatal brain, neurogenesis
Ämneskategorier Neurovetenskap

Sammanfattning

Regenerative responses after hypoxia-ischemia (HI) were investigated in the immature (P9) and juvenile (P21) mouse striatum and cortex by postischemic 5-bromo-2-deoxyuridine labeling and phenotyping of labeled cells 4 weeks later. HI stimulated the formation of new cells in striatum and cortex in immature, growing brains (P9), but when brain growth was finished (P21) proliferation could be stimulated only in striatum, not in cortex. However, the relative increase was higher in P21 (460%) than P9 striatum (50%), though starting from a lower level at P21. Starting from this lower level, HI-induced proliferation in P21 striatum reached the same level as in P9 striatum, but not higher. Phenotyping revealed that low levels of neurogenesis were still present in nonischemic P9 cortex and striatum, but only in striatum at P21. Ischemia-induced neurogenesis was found only in P9 striatum. Ischemia-induced gliogenesis occurred in P9 and P21 striatum as well as P9 cortex, but not in P21 cortex. Hence, the regenerative response was stronger in striatum than cortex, and stronger in P9 than P21 cortex. The biggest ischemia-induced change was the 49-fold increase in P21 striatal microglia, and this was accompanied by increased inflammation, as judged by the size and numbers of CCL2- and interleukin-18-positive cells.Journal of Cerebral Blood Flow & Metabolism advance online publication, 5 November 2008; doi:10.1038/jcbfm.2008.124.

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