Evidence for a Role of Second Pathophysiological Stress in Prevention of Delayed Neuronal Death in the Hippocampal CA1 Region

Bürda, Jozef; Matiasova, Milina; Gottlieb, Miroslav; Danielisová, Viera; Némethová, Miroslava; García, L.; Salinas, Matilde; Burda, Rastislav

doi:10.1007/s11064-005-8510-z

Cited by 54 publications

(57 citation statements)

References 67 publications

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“…It has also been reported that systemic 3-NP administration produces oxidized proteins in the striatum and cortex as well as massive loss Fontaine 2000). Researchers also confirmed 3-NP-induced lesions and oxidative damage in hippocampus (Rodríguez-Martínez et al 2004;Silva et al 2007;Karanian et al 2006;Burda et al 2005). Turan and coworkers reported that chemical preconditioning with 3-NP reduces infarct size via a mechanism that may involve increased bioavailability of NO and decreased ONOOformation (Turan et al 2006).…”

Section: Discussionmentioning

confidence: 78%

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Kumar

2009

Psychopharmacology

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Section: Discussionmentioning

confidence: 78%

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Kumar

2009

Psychopharmacology

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“…Process of apoptosis-like delayed neuronal death manifesting practically 3 days after ischemia can be reversed by sublethal stress stimulus, delayed, protein synthesis dependent, postconditioning, used 2 days after ischemia (Burda et al 2005Danielisova et al 2006Danielisova et al , 2008.…”

Section: Introductionmentioning

confidence: 99%

Postconditioning and Anticonditioning: Possibilities to Interfere to Evoked Apoptosis

et al. 2009

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The aim of this study was to validate the ability of postconditioning, used 2 days after kainate intoxication, to protect selectively vulnerable hippocampal CA1 neurons against delayed neuronal death. Kainic acid (8 mg/kg, i.p.) was used to induce neurodegeneration of pyramidal CA1 neurons in rat hippocampus. Fluoro Jade B, the specific marker of neurodegeneration, and NeuN, a specific neuronal marker were used for visualization of changes 7 days after intoxication without and with delayed postconditioning (norepinephrine, 3.1 mumol/kg i.p., 2 days after kainate administration) and anticonditioning (Extract of Ginkgo biloba, 40 mg/kg p.o used simultaneously with kainate). Morris water maze was used on 6th and 7th day after kainate to test learning and memory capabilities of animals. Our results confirm that postconditioning if used at right time and with optimal intensity is able to prevent delayed neuronal death initiated not only by ischemia but kainate intoxication, too. The protective effect of repeated stress-postconditioning was suppressed if extract of Ginkgo biloba (EGb 761, 40 mg/kg p.o.) has been administered together with kainic acid. It seems that combination of lethal stress and antioxidant treatment blocks the activation of endogenous protecting mechanism known as ischemic tolerance, aggravates neurodegeneration and, after repeated stress is able to cause cumulative damage. This observation could be very valuable in situation when the aim of treatment is elimination of unwanted cell population from the organism.

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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

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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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Evidence for a Role of Second Pathophysiological Stress in Prevention of Delayed Neuronal Death in the Hippocampal CA1 Region

Cited by 54 publications

References 67 publications

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Postconditioning and Anticonditioning: Possibilities to Interfere to Evoked Apoptosis

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

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