Ischemic depolarization monitoring: evaluation of protein synthesis in the hippocampal CA1 after brief unilateral ischemia in a gerbil model

Sorimachi, Takatoshi; Abé, Hiroshi; Takeuchi, Shigekazu; Tanaka, Ryuichi

doi:10.3171/jns.2002.97.1.0104

Cited by 8 publications

(8 citation statements)

References 28 publications

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“…Second, it has been shown that cerebral ischemia causes long-lasting inhibition of protein synthesis despite recovery of energy metabolism (Olsson et al, 2003). This latter point was highlighted in a study showing that gerbils that underwent sublethal ischemia needed a 7-day recirculation period before protein synthesis in hippocampal neurons returned to a normal level (Sorimachi et al, 1999, 2002). Hence, we used a 7-day post-ischemia recovery period to ensure maturation of delayed neuronal death.…”

Section: Discussionmentioning

confidence: 97%

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Kibler

Koehler

et al. 2008

Neuroscience

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Transient global cerebral ischemia causes delayed neuronal death in the hippocampal CA1 region. It also induces an increase in cyclooxygenase 2 (COX-2), which generates several metabolites of arachidonic acid, known as prostanoids, including prostacyclin (PGI2). To determine the role of the PGI2 receptor (IP) in post-ischemic delayed cell death, wild-type and IP knockout (IP−/−) C57Bl/6 mice were subjected to 12-min bilateral common carotid artery occlusion or sham surgery, followed by 7 days of reperfusion. In the sham-operated mice, no statistical difference in CA1 hip-pocampal neuronal density was observed between the wild-type (2836±18/mm2) and IP−/− (2793±43/mm2) mice. Interestingly, in animals subjected to ischemia, surviving neuronal density in wild-type mice decreased to 50.5±7.9% and that of IP−/− mice decreased to 23.0±4.5% of their respective sham-operated controls (P<0.05). The results establish a role for the IP receptor in protecting pyramidal hippocampal neurons after this global ischemic model and suggest that IP receptor agonists could be developed to prevent delayed pyramidal neuronal cell death.

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Section: Discussionmentioning

confidence: 97%

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Kibler

Koehler

et al. 2008

Neuroscience

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“…Core temperatures were recorded after 30 min and then every day until the mice were sacrificed 7 days later. This post-ischemic recovery period was chosen to ensure maturation of delayed neuronal death because it was previously shown in gerbils that 7 days was required for protein synthesis to return to normal levels (Sorimachi et al, 1999;Sorimachi et al, 2002).…”

Section: Global Ischemiamentioning

confidence: 99%

Optimized protocol to reduce variable outcomes for the bilateral common carotid artery occlusion model in mice

Zhen

Doré

2007

Journal of Neuroscience Methods

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The pre-clinical global ischemia model transient bilateral common carotid artery occlusion addresses the unique cascade of events leading to delayed neuronal cell death. However, the inconsistent occurrence of posterior communicating arteries (PcomA) in mice might cause high outcome variability. To determine a means for reducing variability, CD1 mice were subjected to bilateral common carotid artery occlusion for 12 to 40 min. Occlusion duration ≥18 min was applied to mice with bilateral regional cerebral blood flow (rCBF) ≥10% of baseline at 2.5 min of ischemia. However, only groups with ischemic duration ≤18 min were used for statistical analysis because of the high mortality in the other groups. After 7 days, patency of PcomA and hippocampal neuronal loss in the CA1 subfield were evaluated. Outcome variability was reduced when hemispheres containing PcomA were excluded from analysis; ischemic outcome was not affected by the presence of a contralateral PcomA. Extending ischemic duration based on rCBF did not reduce outcome variability because the initial rCBF could not reliably predict PcomA. Therefore, after an optimal ischemic duration, evaluating hippocampal injury in each hemisphere independently according to the existence of PcomA is an effective and reliable method to obtain consistent results in this pre-clinical mouse model.

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“…Thus, the use of inhibitors of protein synthesis as inducers of cell death allows the isolated analysis of the execution pathways of cell death. Furthermore, analysis of cell death induced by translation inhibitors may be of clinical relevance, because inhibition of protein synthesis occurs in neurons during ischemia, immediately upon reperfusion and persists particularly in regions known to suffer extensive cell death (55)(56)(57). It should be noted that, within the time frame examined in our model, cell death following inhibition of protein synthesis is restricted to a specific population of cells (39), and therefore does not represent a trivial metabolic effect.…”

Section: Caspase-9 Induces An Alternative Pathway Of Cell Death Inmentioning

confidence: 99%

Alternative Programs of Cell Death in Developing Retinal Tissue

Guimarães

Benchimol

Amarante-Mendes

et al. 2003

Journal of Biological Chemistry

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We examined cell death in developing retinal tissue, following inhibition of protein synthesis, which kills undifferentiated post-mitotic cells. Ultrastructural features were found of both apoptosis and autophagy. Only approximately half of the degenerating cells were either terminal dUTP nick-end labeling (TUNEL)-positive or reacted with antibodies specific for activated caspases-3 or -9. Bongkrekic acid completely inhibited any appearance of cell death, whereas inhibitors of autophagy, caspases-9 or -3, prevented only TUNEL-positive cell death. Interestingly, inhibition of caspase-6 blocked TUNEL-negative cell death. Simultaneous inhibition of caspases-9 and -6 prevented cell death almost completely, but degeneration dependent on autophagy/ caspase-9 still occurred under inhibition of both caspases-3 and -6. Thus, inhibition of protein synthesis induces in the developing retina various post-translational, mitochondria-dependent pathways of cell death. Autophagy precedes sequential activation of caspases-9 and -3, and DNA fragmentation, whereas, in parallel, caspase-6 leads to a TUNEL-negative form of cell death.

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Ischemic depolarization monitoring: evaluation of protein synthesis in the hippocampal CA1 after brief unilateral ischemia in a gerbil model

Cited by 8 publications

References 28 publications

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Optimized protocol to reduce variable outcomes for the bilateral common carotid artery occlusion model in mice

Alternative Programs of Cell Death in Developing Retinal Tissue

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