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Hypoxic-ischemic encephalopathy (HIE) results in permanent damage of the central nervous system that may result in neonatal death or developmental disorders. 20% – 30% of infants with HIE die in the neonatal period, and 33% – 50% of survivors demonstrate permanent neurodevelopmental abnormalities, such as cerebral palsy and mental retardation. It was shown recently that group II metabotropic glutamate...
INTRODUCTION: Birth asphyxia results in serious damage of central nervous system or neonatal death. It was shown recently that group II metabotropic glutamate receptors (mGluR2/3) activation results in neuroprotection but the exact mechanism of this effect is not clear. AIM(S): The aim of present study was to investigate whether neuroprotective effect of mGluR2/3 activation is connected with inhibition...
There are alarming reports on cytotoxicity of the brominated flame retardant tetrabromobisphenol A (TBBPA) in the in vitro cellular models, that seem to be mediated by increases in the intracellular calcium concentration ([Ca2+] i) and oxidative stress. Still, the mechanisms of both these phenomena, their mutual cause‑and‑effect relationships and implication in the TBBPA-induced neuronal death are...
Previous studies have demonstrated that repeated submission of rats to mild hypobaric hypoxia reduces the persistent behavioral and hormonal depressive symptoms induced by exposure to footshock in the learned helplessness paradigm. The aim of this study was to determine whether hypoxic preconditioning of mice can also induce antidepressant- and anxiolyticlike effects that are detectable with the other...
BACKGROUND AND AIMS: Influx of calcium ions (Ca2+) into neurons after stimulation of glutamate receptors is a crucial step in intracellular cascade of memory formation. Recent findings showed the existence of additional mechanism involved in intracellular Ca2+ increase and triggered not by external signal but by internal signals like increase of Ca2+ within the cell and activation of G protein coupled...
BACKGROUND AND AIMS: The results of early studies suggested a role of glutamate receptors in the mechanism of increases in intracellular Ca2+ concentration ([Ca2+]i ) and cytotoxicity induced by the brominated flame retardant, tetrabromobisphenol-A (TBBPA). Although now interest has focused mainly on TBBPA-induced Ca2+ release from intracellular stores, here we revisited the former issue and tested...
BACKGROUND AND AIMS: Perinatal asphyxia is characterized by clinical and laboratory evidence of acute brain injury due to asphyxia. It was shown that mGluR2/3 activation before or after ischemic insult results in neuroprotection but the exact mechanism of this effect is not clear. The aim of present study was to investigate whether mGluR2/3 activation after hypoxia-ischemia (HI) reduces brain damage...
BACKGROUND AND AIMS: Perinatal hypoxia ischemia (HI) is a frequent cause of neonatal brain injury. The aim of present study was to investigate the effect of combining HBO or HH with memantine on HI evoked apoptosis and on Bcl-2, Bax and HIF-1α expression in hippocampus and cerebral cortex of the brains of neonatal rats. METHODS: HI on 7-day old rats was induced by ligation of ipsilateral common carotid...
Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days...
Encephalopathy caused by birth asphyxia results in significant mortality and long-term morbidity. In our previous studies we proved that HBO reduces brain damage in experimental model of birth asphyxia by almost 60%. The aim of present study was to evaluate the effect of hyperbaric oxygen (HBO) on reactive oxygen species (ROS) production and antioxidative enzymes activities – catalase (CAT) and glutathione...
It is known that mGluRs group I (mGluR1 and mGluR5) are involved in memory consolidation and reconsolidation probably by local protein synthesis regulation. One of the consequences of group I mGluRs activation is the synthesis of new proteins that play important role in memory consolidation and reconsolidation – NCAM and CaMKII, and also FMRP, that plays an important role in the mRNA transport and...
It is known, that group I metabotropic glutamate receptors (mGluRs) are involved in memory consolidation and reconsolidation. The Ca2+ signal derived from IP3 receptors (IP3R) stimulation via mGluRs activation, initiates protein synthesis that is necessary for complete memory consolidation, whereas it is suggested that during retrieval and reconsolidation of memory other mGluR1/5 triggered mechanisms...
1,2,3,4,-Tetrahydroisochinolines (TIQ) are endogenous substances present in brain in low concentrations. Several TIQ derivatives are neurotoxic producing a Parkinson’s syndrome. In turn 1-methyl-1- ,2,3,4,-tetrahydroisochinoline (1MeTIQ) was found to reduce neuronal death in various models of neurotoxicity. Our previous results revealed that 1MeTIQ reduces excitotoxicity in the primary culture of...
Various endogenous teterahydroisochinoline derivatives present in the mammalian brain have been considered as neurotoxic substances. However 1-methyl-1,2,3,4-tetrahydroisochinoline (1MeTIQ) is known for its mild neuroprotective potential of the unclear mechanism. On the one hand 1MeTIQ exhibits anti-dopaminergic activity and reduces the neurotoxic effects of MPTP and rotenone, decreasing also the...
Alternative methods of the therapy in the brain ischemia such as preconditioning seem more interesting because of the lack of the clinical applicable effective pharmacological neuroprotection. The role of NMDA receptor activation in triggering of this phenomenon was suggested, but it is not clear. Our recent in vitro studies (Kuszczyk et al. 2010) disclosed tolerance to the excitotoxic challenge by...
Lack of the clinically applicable effective pharmacological neuroprotection in different forms of brain ischemia triggers increasing interest in alternative methods of therapy, including induction of brain tolerance by pre- and postconditioning. It is known for a long time that hypoxic preconditioning reduces brain damage in the rat model of perinatal asphyxia (Vannucci et al., 1998, Cantagrel et...
Lack of the clinically effective pharmacological neuroprotection in different forms of brain ischemia increased the interest in alternative methods of therapy, like hypothermia or induction of brain tolerance by pre- and post-conditioning. The hyperbaric oxygen (HBO) therapy (2.5 atm) applied after ischemia or traumatic brain injury is one of the proposed but still controversial methods. The aim of...
Induction of short ischemic episodes after the stroke can be neuroprotective. Hypoxia was also suggested as the factor producing neuroprotection in the animal brain. Therefore in our studies we aimed to test if normobaric hypoxia (10% of oxygen) induced after ischemia could prevent neuronal loss. The model of hypoxia-ischemia (H-I) in 7-days old rats and the model of global forebrain ischemia in Mongolian...
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