Mechanism and pathogenesis of ischemia-induced neuronal damage

Hara, Hideaki; Sukamoto, Takayuki; Kogure, Kyuya

doi:10.1016/0301-0082(93)90009-h

Cited by 120 publications

(45 citation statements)

References 180 publications

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“…In these cells, a response to DNA damage involves nucleotide excision repair and, if this is undertaken in the presence of BrdU, the cell can incorporate the nucleotide (Kuan et al, 2004). Hippocampal CA1 neurons are particularly sensitive and undergo selective, delayed degeneration in response to transient global ischemia (Kirino, 1982;Hara et al, 1993;Ferrer et al, 1997). Accordingly, we found a profound and selective loss of neurons, evaluated by Nissl staining (not shown) and NeuN labelling in this region 72 h after ischemia induction.…”

Section: Discussionmentioning

confidence: 67%

“…It is known that transient global cerebral ischemia leads to delayed cell death of CA1 pyramidal neurons of the hippocampus in adult gerbils (Kirino, 1982;Schmidt-Kastner and Freund, 1991;Hara et al, 1993;Ferrer et al, 1997;Horiguchi et al, 2002), and that brain ischemia increases neurogenesis in the DG of the hippocampus of rodents including gerbils (Takagi et al, 1999;Sharp et al, 2002;Kokaia and Lindvall, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Ischemia induces cell proliferation and neurogenesis in the gerbil hippocampus in response to neuronal death

Salazar-Colocho

Lanciego

Rı́o

et al. 2008

Neuroscience Research

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We studied hippocampal cellular proliferation and neurogenesis processes in a model of transient global cerebral ischemia in gerbils by labelling dividing cells with 5 0 -Bromo-2 0 -deoxyuridine (BrdU). Surrounding the region of selective neuronal death (CA1 pyramidal layer of the hippocampus), an important increase in reactive astrocytes and BrdU-labelled cells was detected 5 days after ischemia. A similar result was found in the dentate gyrus (DG) 12 days after ischemia. The differentiation of the BrdU+ cells was investigated 28 days after BrdU administration by analyzing the morphology, anatomic localization and cell phenotype by triple fluorescent labelling (BrdU, adult neural marker NeuN and DNA marker TOPRO-3) using confocal laser-scanning microscopy. This analysis showed increased neurogenesis in the DG in case of ischemia and triple positive labelling in some newborn cells in CA1. Seven brain hemispheres from gerbils subjected to ischemia did not develop CA1 neuronal death; hippocampus from these hemispheres did not show any of the above mentioned findings. Our results indicate that ischemia triggers proliferation in CA1 and neurogenesis in the DG in response to CA1 pyramidal neuronal death, independently of the reduced cerebral blood flow or the cell migration from subventricular zone (SVZ). #

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Section: Discussionmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Ischemia induces cell proliferation and neurogenesis in the gerbil hippocampus in response to neuronal death

Salazar-Colocho

Lanciego

Rı́o

et al. 2008

Neuroscience Research

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show abstract

“…Excitotoxic effects of hypoxia and ischemia are attributable, in part, to excessive release of glutamate (Hara et al, 1993;Schroder et al, 1999). Under these conditions, the concentration of adenosine available increases and activates A1Rs to reduce excitotoxicity (Fowler, 1989;Simpson et al, 1992;Katchman and Hershkowitz, 1993;Sweeney, 1997).…”

Section: A2 a Rs Enhance Ipsps But Not Epspsmentioning

confidence: 99%

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

Brooke

Deuchars²,

Deuchars³

2004

J. Neurosci.

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“…In a brief period of global cerebral ischemia, damage occurred in selectively vulnerable regions of the brain (21). In the gerbil, a 5-min ischemic insult produced substantial damage to the CA1 sector of the hippocampus (6,36).…”

Section: Neuroprotective Propertiesmentioning

confidence: 99%