Global ischemia can cause DNA fragmentation indicative of apoptosis in rat brain

MacManus, J. P.; Buchan, Alastair; Hill, Irene E.; Rasquinha, Ingrid; Preston, Edward

doi:10.1016/0304-3940(93)90864-h

Cited by 455 publications

(179 citation statements)

References 12 publications

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“…We have also observed that young (seven days in vitro) cultured cortical neurons, which express few glutamate receptors, die by apoptosis when confronted with glucose deprivation in the absence of glutamate antagonists (unpublished data). Our results thus support the emerging idea that neuronal apoptosis may occur after ischemic insults in vivo 22,23,25,30 and add the notions of parallel occurrence and hierarchy. Present experiments are notable in delineating parallel necrosis and apoptosis induced by a single insult in the same neurons.…”

supporting

confidence: 86%

Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro

et al. 1995

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supporting

confidence: 86%

Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro

et al. 1995

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“…However, there is now compelling evidence in a number of neuronal cell types, including CGC, that apoptosis as well as necrosis underlie the death of neurones after an excitotoxin exposure (Kure et al, 1991;Heron et al, 1993;Linnik et al, 1993;MacManus et al, 1993MacManus et al, , 1994Ankarcrona et al, 1995; FIG. 8.…”

Section: Figmentioning

confidence: 99%

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

Staton

Bristow

1997

Journal of Neurochemistry

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Abstract:The neurotoxic properties of the dietary excitotoxins /3-N-methylamino-L-alanine and~3-N-oxalylamino-L-alanine have been studied in rat cerebellar granule cells and compared with those of glutamate. Glutamate caused dose-dependent death of cerebellar granule cells after a 30-min exposure when viability was assessed 24 h later. ß-N-Methylamino-L-alanine and /3-N-oxalylamino-L-alanine, however, were toxic only after 24 or 48 h of exposure. The neurotoxic effects of ß-N-methylaminO-L-alanine were blocked by D(-)-2-amino-5-phosphonopentanoic acid, and those of ß-N-oxalylamino-Lalanine were blocked by kynurenic acid, which demonstrated that these excitotoxins caused cerebellar granule cell death through the activation of glutamate receptors.

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“…The resulting intracellular Ca 2+ overload activates Ca2+-mediated downstream mechanisms and eventually neuronal death [2]. The type of cell death in glutamatetreated neurons has been studied both in primary cultures in vitro [3][4][5] and in ischemia models in vivo [6][7][8][9], and it has been demonstrated that both necrosis and apoptosis take place. Necrosis leads to rapid destruction of neurons associated with cellular and organelle swelling, energy depletion and membrane destruction.…”

Section: Introductionmentioning

confidence: 99%

“…The degree of apoptosis occurring in vivo is frequently underestimated, since secondary necrosis and phagocytosis of apoptotic cells take place [13]. However, an apoptotic component of cell death in the ischemic brain has been suggested by experiments showing DNA fragmentation in the ischemic tissue [6][7][8][9]. We have recently shown that both ne- [5].…”

Section: Introductionmentioning

confidence: 99%

Calcineurin and mitochondrial function in glutamate‐induced neuronal cell death

et al. 1996

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We have previously reported that glutamate can trigger a succession of necrosis and apoptosis in cerebellar granule cells (CGC). Since specific blockers of the N-methyl-aaspartate (NMDA) receptor channel prevented both types of cell death, the role of Ca2+-dependent processes in the initiation of glutamate toxicity was further investigated. We examined the possible involvement of mitochondria and the role of the Ca2÷/ calmodulin-regulated protein phosphatase, calcineurin, in the development of either type of cell death. Cyclosporin A and the more selective calcineurin inhibitor, FK-506, prevented the development of both early necrosis and delayed apoptosis. In addition, cyclosporin A prevented the collapse of mitochondrial membrane potential observed during the exposure to glutamate and the concomitant necrotic phase. When CsA was added immediately after glutamate removal, it also prevented delayed apoptosis of neurons that bad survived the necrotic phase. Altogether, these results suggest the involvement of calcineurin and a role for mitochondrial decnergization as early signals in neuronal apoptosis induced by glutamate.

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Global ischemia can cause DNA fragmentation indicative of apoptosis in rat brain

Cited by 455 publications

References 12 publications

Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro

Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

Calcineurin and mitochondrial function in glutamate‐induced neuronal cell death

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