Apoptosis associated DNA fragmentation in epileptic brain damage

Pollard, H.; Cantagrel, S.; Charriaut‐Marlangue, Christiane; Moreau, J.; Ari, Y. Ben

doi:10.1097/00001756-199405000-00009

Cited by 104 publications

(31 citation statements)

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“…The domination of order even late after the initial ischemic period strengthens the suggestion, despite the absence of morphological evidence, that ischemic neurons are using some component of the apoptotic machinery. The accu mulating evidence in support of this conclusion from our own studies and those in other laborato ries (Heron et al, 1993;Linnik et al, 1993;Mac Manus et al, 1993;Okamoto et al, 1993;Tominaga et al, 1993;MacManus et al, 1994;Sei et al, 1994), now also including studies of epilepsy (Pollard et al, 1994), indicates that such research might lead to discoveries of new molecular targets for drug inter vention in the debilitating postischemic neuronal degeneration of stroke.…”

Section: N H S N H Sn Hs N H Ssupporting

confidence: 72%

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

MacManus¹,

Hill²,

Preston³

et al. 1995

J Cereb Blood Flow Metab

113

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Summary:The time course of appearance of cells with DNA damage was studied in rats following transient se vere forebrain ischemia. This DNA damage could be de tected by in situ end-labeling on brain sections. The breaks in DNA appeared selectively by day I in the stri atum and later in the CAl region of the hippocampus. It was possible by double labeling to show that there was no DNA damage in astrocytes. The DNA breaks consisted of laddered DNA fragments indicative of an ordered ap optotic type of internucleosomal cleavage, which per sisted without smearing for up to 7 days of reperfusion. In

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Section: N H S N H Sn Hs N H Ssupporting

confidence: 72%

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

MacManus¹,

Hill²,

Preston³

et al. 1995

J Cereb Blood Flow Metab

113

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“…6,7,27 However, there is some evidence for an apoptotic pathway of neuron death, as demonstrated by the appearance of certain morphological and biochemical features characteristic of apoptosis. [28][29][30][31][32][33] Emerging data support the idea that apoptosis and necrosis in vivo are not distinct, clear-cut pathways, but rather represent a morphological continuum of neuronal death processes.…”

Section: Discussionmentioning

confidence: 87%

HSV-mediated delivery of virally derived anti-apoptotic genes protects the rat hippocampus from damage following excitotoxicity, but not metabolic disruption

2002

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“…Necrosis usually deletes groups or clusters of cells and includes loss of membrane integrity, cellular swelling, and lysis as well as activation of brain microglia and astrocytes. However, recent studies have shown that neurons also die via apoptosis following excitotoxic injury (9)(10)(11)(12)(33)(34)(35)(36)(37)(38). Apoptosis involves specific deletion of single cells and is characterized by cell shrinkage, plasma, and nuclear membrane blebbing and budding off of fragments known as apoptotic bodies, chromatin condensation, and endonuclease-mediated DNA cleavage (39)(40)(41).…”

Section: Discussionmentioning

confidence: 99%

“…Seizure-induced cell death has traditionally been discussed in the context of excitotoxic mechanisms and degeneration through necrosis (7,8). More recently, however, it has been shown that apoptosis contributes to the degeneration following status epilepticus in rats (9)(10)(11)(12). Even if longer periods of seizure activity, lasting for hours, invariably cause death of hippocampal neurons, it is unclear if single or intermittent seizures, with a duration in the range of minutes, can lead to neuronal damage.…”

mentioning

confidence: 99%

Apoptosis and proliferation of dentate gyrus neurons after single and intermittent limbic seizures

Bengzon

Kokaia

Elmér

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

710

422

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Neuronal apoptosis was observed in the rat dentate gyrus in two experimental models of human limbic epilepsy. Five hours after one hippocampal kindling stimulation, a marked increase of in situ terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) of fragmented DNA was observed in nuclei located within and on the hilar border of the granule cell layer and in the polymorphic region. Forty kindling stimulations with 5-min interval produced higher numbers of labeled nuclei compared with one stimulation. The increase of TUNEL-positive nuclei was prevented by the protein synthesis inhibitor cycloheximide but not affected by the N-methyl-D-aspartate receptor antagonist MK-801. Kainic acidinduced seizures lead to a pattern of labeling in the hippocampal formation identical to that evoked by kindling. A large proportion of cells displaying TUNEL-positive nuclei was doublelabeled by the neuron-specific antigen NeuN, demonstrating the neuronal identity of apoptotic cells. Either 1 or 40 kindling stimulations also gave rise to a marked increase of the number of cells double-labeled with the mitotic marker bromodeoxyuridine and NeuN in the subgranular zone and on the hilar border of the dentate granule cell layer. The present data show that single and intermittent, brief seizures induce both apoptotic death and proliferation of dentate gyrus neurons. We hypothesize that these processes, occurring early during epileptogenesis, are primary events in the development of hippocampal pathology in animals and possibly also in patients suffering from temporal lobe epilepsy.

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Apoptosis associated DNA fragmentation in epileptic brain damage

Cited by 104 publications

References 0 publications

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

HSV-mediated delivery of virally derived anti-apoptotic genes protects the rat hippocampus from damage following excitotoxicity, but not metabolic disruption

Apoptosis and proliferation of dentate gyrus neurons after single and intermittent limbic seizures

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