Delayed Postconditionig Initiates Additive Mechanism Necessary for Survival of Selectively Vulnerable Neurons After Transient Ischemia in Rat Brain

Bürda, Jozef; Danielisová, Viera; Némethová, Miroslava; Gottlieb, Miroslav; Matiasova, Milina; Domoráková, Iveta; Mechírová, Eva; Feriková, Marianna; Salinas, Matilde; Burda, Rastislav

doi:10.1007/s10571-006-9036-x

Cited by 101 publications

(88 citation statements)

References 59 publications

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“…Earlier, it has been reported that IPoC reduces I/R induced hippocampal damage. 41,42) Further, IPoC also attenuated I/R induced impairment in sensorimotor functions, which may possibly due to its protective effects on cortical neurons and striatum. Earlier, IPoC has been documented to prevent I/R induced damage to cortical neurons and striatum.…”

Section: Discussionmentioning

confidence: 87%

“…Earlier, IPoC has been documented to prevent I/R induced damage to cortical neurons and striatum. 42) Collectively, these protective effects of IPoC on hippocampus, cortex and striatum were manifested in the form of reduction in cerebral infarct size, measured by both volume and weight methods. Moreover, there was a direct correlation between the degree of infarction and impairment in behavioral functions (memory and sensorimotor), as already reported in earlier papers from our laboratory.…”

Section: Discussionmentioning

confidence: 99%

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Possible Role of Opioids and KATP Channels in Neuroprotective Effect of Postconditioning in Mice

Pateliya

Singh

Jaggi

2008

Biological & Pharmaceutical Bulletin

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The present study was designed to investigate the possible role of opioids and K ATP channels in ischemic postconditioning-induced reversal of global cerebral ischemia and reperfusion (I/R) induced neuronal injury. Mice were subjected to global ischemia by bilateral carotid artery occlusion for 10 min followed by reperfusion for 24 h, to produce neuronal injury. Ischemic postconditioning was induced by three episodes of carotid artery occlusion and reperfusion of 10 s each, immediately after global ischemia. Morphine postconditioning was induced by administration of morphine (5 mg/kg i.v.), 5 min prior to reperfusion. Naloxone (5 mg/kg i.v.), opioid receptor antagonist, and glibenclamide (5 mg/kg i.v.), K ATP channel blocker were administered 10 min before global ischemia. Extent of cerebral injury was assessed by measuring cerebral infarct size using triphenyl tetrazolium chloride (TTC) staining. Short-term memory was evaluated using the elevated plus maze test, while degree of motor incoordination was evaluated using inclined beam-walking, rota-rod and lateral push tests. Bilateral carotid artery occlusion followed by reperfusion resulted in significant increase in infarct size, impairment in short-term memory and motor co-ordination. Ischemic/morphine postconditioning significantly attenuated I/R induced neuronal injury and behavioural alterations. Pretreatments with naloxone and glibenclamide attenuated the neuroprotective effects of ischemic/morphine postconditioning. It may be concluded that ischemic/morphine postconditioning protects I/R induced cerebral injury via activating opioid receptor and K ATP channel opening.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Possible Role of Opioids and KATP Channels in Neuroprotective Effect of Postconditioning in Mice

Pateliya

Singh

Jaggi

2008

Biological & Pharmaceutical Bulletin

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“…1 To date, early brain ischemic postconditioning has been first reported in focal ischemia, [3][4][5] then delayed postconditioning against focal 6 and in global ischemia. 7 We have previously shown that hypoxic preconditioning (8% O 2 , 1 hour) performed 24 hours before focal cerebral ischemia in adult mice protects the brain. 10 Furthermore, we reported in vitro a neuroprotective effect of hypoxic preconditioning (0.1% O 2 , 1 hour) when performed 24 hours before OGD on neurons.…”

Section: Discussionmentioning

confidence: 98%

“…[3][4][5] More delayed ischemic postconditioning, starting 6 hours and 24 hours after focal and global cerebral ischemia, respectively, has been also recently described. 6,7 Whereas the molecular mechanisms of cerebral ischemic preconditioning were addressed in many studies, 1 those of postconditioning after focal ischemia were only suggested in a few studies. The protection has been associated with the activation of the protein kinase Akt.…”

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confidence: 99%

Delayed Hypoxic Postconditioning Protects Against Cerebral Ischemia in the Mouse

Leconte

Tixier

Freret

et al. 2009

Stroke

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Background and Purpose-Inspired from preconditioning studies, ischemic postconditioning, consisting of the application of intermittent interruptions of blood flow shortly after reperfusion, has been described in cardiac ischemia and recently in stroke. It is well known that ischemic tolerance can be achieved in the brain not only by ischemic preconditioning, but also by hypoxic preconditioning. However, the existence of hypoxic postconditioning has never been reported in cerebral ischemia. Methods-Adult mice subjected to transient middle cerebral artery occlusion underwent chronic intermittent hypoxia starting either 1 or 5 days after ischemia and brain damage was assessed by T2-weighted MRI at 43 days. In addition, we investigated the potential neuroprotective effect of hypoxia applied after oxygen glucose deprivation in primary neuronal cultures. Results-The present study shows for the first time that a late application of hypoxia (5 days) after ischemia reduced delayed thalamic atrophy. Furthermore, hypoxia performed 14 hours after oxygen glucose deprivation induced neuroprotection in primary neuronal cultures. We found that hypoxia-inducible factor-1␣ expression as well as those of its target genes erythropoietin and adrenomedullin is increased by hypoxic postconditioning. Further studies with pharmacological inhibitors or recombinant proteins for erythropoietin and adrenomedullin revealed that these molecules participate in this hypoxia postconditioning-induced neuroprotection. Conclusions-Altogether, this study demonstrates for the first time the existence of a delayed hypoxic postconditioning in cerebral ischemia and in vitro studies highlight hypoxia-inducible factor-1␣ and its target genes, erythropoietin and adrenomedullin, as potential effectors of postconditioning. Key Words: adrenomedullin Ⅲ erythropoietin Ⅲ hypoxia Ⅲ ischemia Ⅲ postconditioning I schemic or hypoxic preconditioning is a sublethal stress able to reduce ischemia-induced injury when applied before ischemia, 1 a phenomenon called ischemic tolerance. Understanding the mechanisms underlying this preconditioning-induced tolerance might allow identification of new therapeutic targets. However, its application is not clinically feasible because the occurrence of stroke is hardly predictable. By analogy with preconditioning, postconditioning represents another promising strategy to modulate brain ischemic damage. Based on studies in the heart, 2 ischemic postconditioning was defined as a repetitive series of brief interruptions of reperfusion applied after ischemia that confers neuroprotection, probably by attenuating reperfusion injury. Inspired from these studies, the neuroprotective effect of ischemic postconditioning applied immediately after the ischemic insult has been reported in models of focal cerebral ischemia in the rat. [3][4][5] More delayed ischemic postconditioning, starting 6 hours and 24 hours after focal and global cerebral ischemia, respectively, has been also recently described. 6,7 Whereas the molecular mechanisms of cer...

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“…However, the prevention of inhibition of translation does not assure survival of CA1 neurons (Burda et al 2003). But endogenous defense mechanism known as ischemic tolerance inevitably needs recovery of protein synthesis (Burda et al 2005(Burda et al , 2006.…”

Section: Discussionmentioning

confidence: 99%

Effect of L-carnitine on postischemic inhibition of protein synthesis in the rat brain

Bürda¹,

M²,

Danielisová³

et al. 2009

gpb

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Abstract. The purpose of this study was to investigate effects of carnitine administration on protein synthesis recovery after transient cerebral ischemia. Rats received L-carnitine in two doses of 16 mmol/kg i.p. 15 min before ischemia and just on the onset of reperfusion. Transient forebrain ischemia was induced by 4-vessel occlusion for 15 min, followed by 30 min or 7 days of reperfusion. Protein synthesis rate, reinitiation ability and neurodegeneration in the frontal cortex and hippocampus were measured by the incorporation of radioactively labelled leucine into polypeptide chains in postmitochondrial supernatants and by Fluoro-Jade B staining.A protective effect was observed, on protein synthesis as well as the number of surviving neurons, in the L-carnitine-treated groups. Our results indicate that L-carnitine can exert a protective effect in the development of reperfusion-induced injury. L-carnitine significantly reduced the ischemia/reperfusion-induced inhibition of translation and neurodegeneration in the neocortex as well as in the highly sensitive hippocampus and dorsolateral striatum. We expect that the ability of L-carnitine to keep translational machinery on facilitates efficacy of postischemic remodulation of gene expression.

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Delayed Postconditionig Initiates Additive Mechanism Necessary for Survival of Selectively Vulnerable Neurons After Transient Ischemia in Rat Brain

Cited by 101 publications

References 59 publications

Possible Role of Opioids and KATP Channels in Neuroprotective Effect of Postconditioning in Mice

Possible Role of Opioids and KATP Channels in Neuroprotective Effect of Postconditioning in Mice

Delayed Hypoxic Postconditioning Protects Against Cerebral Ischemia in the Mouse

Effect of L-carnitine on postischemic inhibition of protein synthesis in the rat brain

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