Qualitative and quantitative estimates of apoptosis from birth to senescence in the rat brain

White, L.; Barone, Stanley

doi:10.1038/sj.cdd.4400816

Cited by 84 publications

(51 citation statements)

References 53 publications

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“…Comparable number of FJB+ cells were found in P7 control and hypoglycemia groups, suggesting that acute hypoglycemia was not associated with neuronal injury at this age. The FJB+ cells at this age likely reflect the programmed cell death that is active until P10 [27,39]. Finally, consistent with a previous study in adult rats [35], the hypothalamus was spared in all ages, likely secondary to its low glucose requirements [22].…”

Section: Discussionsupporting

confidence: 74%

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

et al. 2008

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Acute hypoglycemia is associated with neuronal injury in the mature human and rodent brains. Even though hypoglycemia is a common metabolic problem during development, its effects on the developing brain are not well understood. To characterize the severity of regional brain injury, postnatal day (P) 7, P14, P28 (N=20-30/age) and adult rats (N=8-12) were subjected to acute hypoglycemia of equivalent severity and duration (mean blood glucose concentration: 30.0±0.1 mg/ dL for 210 min). Neuronal injury in the cerebral cortex, striatum, hippocampus and hypothalamus was assessed 24 hr, 72 hr and 1 wk later by determining the number of degenerating cells positive for Fluoro-Jade B (FJB+) in the region. Compared with age-matched control, greater number of FJB + cells was present per brain section of P14, P28 and adult hypoglycemia groups (P<0.005, each). The cerebral cortex was more vulnerable than hippocampus and striatum at all three ages (P<0.01). Compared with P28 (131±21) and adult (171±21) rats, fewer FJB+ cells (39±6) per brain section were present in P14 hypoglycemic rats (P<0.01, each). Hypoglycemia was not associated with cell injury in P7 rats. FJB+ cells were absent in the hypothalamus in all four ages. Similar results were present 24 hr post-hypoglycemia, where as analysis at 1 wk demonstrated efficient clearing of FJB + cells in the brain regions of developing rats. Varying the duration of fasting did not alter the severity of regional cell injury. These results suggest that postnatal age influences the regional vulnerability to hypoglycemia-induced neuronal death in the rat brain.

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Section: Discussionsupporting

confidence: 74%

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

et al. 2008

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“…These methods were suitably sensitive to detect cell death in the developing brain, and to study the concentration response of drug-induced DNA fragmentation in vivo [27]. Such techniques based on the use of the whole cell population of the brain structure may be effective for evaluation of the cell death during early life since naturally occurring cell death is not synchronized in different cells and only few such cells could be detected on a single slice of the developing brain tissue at each time moment [26,28]. Traces of DNA fragments present in the brain samples were obviously produced by natural apoptosis in the developing brain [2].…”

Section: Discussionmentioning

confidence: 99%

“…Highly sensitive in situ techniques for detection of DNA fragmentation in a single cell such as TUNEL are capable however to label repairable nicks and do not allow to determine the amount of fragmented DNA in the whole brain structure [25]. Recently several groups used electrophoresis-based approach for densitometry quantification of the typical for apoptosis DNA laddering [16,25,26]. These methods were suitably sensitive to detect cell death in the developing brain, and to study the concentration response of drug-induced DNA fragmentation in vivo [27].…”

Section: Discussionmentioning

confidence: 99%

Region-Specific Interrelations between Apoptotic Proteins Expression and DNA Fragmentation in the Neonatal Rat Brain

Menshanov

Bannova²,

Дыгало³

2006

Neurochem Res

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DNA fragmentation, mRNA and protein levels of Bcl-XL, Bax and caspase-3 were determined to characterize interrelations between expression of these apoptotic markers in the neonatal brain regions. High DNA fragmentation intensity in the cortex was in consonance with the lowest Bcl-XL/Bax expression ratio, the highest procaspase-3 and active caspase-3 levels. Low and intermediate DNA fragmentation levels in the cerebellum and hippocampus respectively were also in a good agreement with apoptotic proteins expression in these structures. In the cortex, hippocampus and cerebellum DNA fragmentation intensity was proportional to the active caspase-3 level. In contrast to these structures, in the brainstem, the lowest level of this protease was accompanied by the highest intensity of DNA fragmentation among the brain regions studied. The data suggest that cell death normally occurring during early postnatal life could be realized in the developing brainstem via caspase-3-independent pathways in animals that express this protease.

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“…Aging and hypoxia are accompanied by decreasing brain volume and cortical weight, as well as in loss of cortical neurons (Masliah et al ., 1993;Zhang et al ., 1995;Brody, 1997;Pakkenberg & Gundersen, 1997;Jernigan et al ., 2001;White & Barone, 2001;Anderton, 2002). Cell counting, performed in haematoxylin-eosin-stained sections on 77 000-µ m 2 fields, shows a reduced density of neurons in hypoxic and normoxic old cerebral cortex, as compared with young in the same experimental conditions (Fig.…”

Section: Resultsmentioning

confidence: 99%

HIF‐1α cytoplasmic accumulation is associated with cell death in old rat cerebral cortex exposed to intermittent hypoxia

Rapino¹,

Bianchi²,

Giulio³

et al. 2005

Aging Cell

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SummaryIntermittent hypoxia, followed by reoxygenation, determines the production of reactive oxygen species (ROS), which may lead to accelerated aging and to the appearance of age-related diseases. The rise in ROS levels might constitute a stress-stimulus activating specific redoxsensitive signalling pathways, so inducing either damaging or protective functions. Here, we report that in old rat cerebral cortex exposed to hypoxia, the accumulation in the cytoplasm of hypoxic inducible factor 1α α α α (HIF-1α α α α ) -the master regulator of oxygen homeostasis -concomitant with p66Shc activation and reduced IkBα α α α phosphorylation is associated with tissue apoptosis or necrosis. In young cerebral cortex, we hypothesize that the hypoxic damage may be reversible, based on our demonstration of elevated HIF-1α α α α levels, combined with a low level of IkBα α α α phosphorylation, a decrease in IAP-1 and a lack of major change in Bcl2 family proteins. These observations are associated with a low level of cell death induced by hypoxia, suggesting that HIF-1α α α α activation in cortical neurons may produce rescue proteins in response to intermittent hypoxia.

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Qualitative and quantitative estimates of apoptosis from birth to senescence in the rat brain

Cited by 84 publications

References 53 publications

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

Region-Specific Interrelations between Apoptotic Proteins Expression and DNA Fragmentation in the Neonatal Rat Brain

HIF‐1α cytoplasmic accumulation is associated with cell death in old rat cerebral cortex exposed to intermittent hypoxia

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