Ischemic Neuronal Damage

Taoufik, Era; Probert, Lesley

doi:10.2174/138161208786848748

Cited by 124 publications

(84 citation statements)

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“…Thus large amounts of ATP can be released into the extracellular space under pathological conditions such as tissue injury, cell lysis, and cell ischemia. 3,108 Under physiological conditions, cytosolic ATP can be released via transmembrane transport in response to receptor activation in both vascular smooth muscle cells and endothelial cells. 96,98,68,123 In most neurons, ATP is stored in vesicles with neurotransmitters and coreleased.…”

Section: +mentioning

confidence: 99%

Spatiotemporal characteristics of calcium dynamics in astrocytes

Kang

Othmer

2009

Chaos: An Interdisciplinary Journal of Nonlinear Science

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Although Ca i2+ waves in networks of astrocytes in vivo are well documented, propagation in vivo is much more complex than in culture, and there is no consensus concerning the dominant roles of intercellular and extracellular messengers ͓inositol 1,4,5-trisphosphate ͑IP 3 ͒ and adenosine-5Ј-triphosphate ͑ATP͔͒ that mediate Ca i 2+ waves. Moreover, to date only simplified models that take very little account of the geometrical struture of the networks have been studied. Our aim in this paper is to develop a mathematical model based on realistic cellular morphology and network connectivity, and a computational framework for simulating the model, in order to address these issues. In the model, Ca i 2+ wave propagation through a network of astrocytes is driven by IP 3 diffusion between cells and ATP transport in the extracellular space. Numerical simulations of the model show that different kinetic and geometric assumptions give rise to differences in Ca i 2+ wave propagation patterns, as characterized by the velocity, propagation distance, time delay in propagation from one cell to another, and the evolution of Ca 2+ response patterns. Calcium "Ca 2+… is one of the most versatile and widely used second-messenger molecules and plays a pivotal role in neurotransmission, muscle contraction, gene expression, and a variety of other intracellular processes. 13,37Because high levels of intracellular calcium are toxic, and because it cannot be degraded as many other signaling molecules are, cells control the intracellular calcium level at around 100 nM (compared to millimolar extracellular levels) by buffering, sequestration in specialized compartments, and by expulsion to the extracellular space.

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Section: +mentioning

confidence: 99%

Spatiotemporal characteristics of calcium dynamics in astrocytes

Kang

Othmer

2009

Chaos: An Interdisciplinary Journal of Nonlinear Science

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“…The ionotropic glutamate receptors are NMDA receptors and AMPA receptors. The cerebral concentration of Glu and Asp can increase too high, which can overactivate the NMDA receptor that can cause various consequences, including the over-activation of protein kinases, endonucleases, phosphoglycerate kinase, and nitric oxide synthase, and the formation of peroxide, thus leading to the degradation of DNA and death of neurons (Taoufik and Probert, 2008). In the present study, we found that the excitatory amino acids Glu, Asp, and Gly increased significantly after DHCA, which was consistent with previous studies (Tseng et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Relative Higher Hematocrit Attenuates the Cerebral Excitatory Amino Acid Elevation Induced by Deep Hypothermic Circulatory Arrest in Rats

Zhu

Zhao

Zheng

et al. 2013

Therapeutic Hypothermia and Temperature Management

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Hemodilution is a commonly used technique in cardiopulmonary bypass (CPB) and deep hypothermic circulation arrest (DHCA). Our previous study showed that lower hematocrit aggravated the brain injury after DCHA. Because the excitatory amino acids are critical pathways of ischemic neuronal damage, the purpose of the present study was to investigate the effects of different degrees of hemodilution on the excitatory amino acid content in different brain areas after DHCA Adult Sprague-Dawley rats were randomly divided into four groups: group I hematocrit (Hct) 10% (H1), group II Hct 20% (H2), group III Hct 30% (H3), and control group (C). All animals except those in the control group underwent DHCA at 18°C for 90 minutes. Different degrees of hemodilution were accomplished by changing the composition and volume of the priming solution used in CPB. High-performance liquid chromatography was used to determine the concentration of glutamate (Glu), aspartate (Asp), glycine (Gly), gamma-aminobutyric acid (GABA), and taurine (Tau) in the cerebral cortex, hippocampus, and thalamus. We found that the concentration of these five amino acids in the hippocampus and cortex were all increased after DHCA. Glu, Asp, and Gly in the hippocampus and cortex were significantly lower in the Hct 30% group than in the other two groups ( p < 0.05). There was no significant difference in the GABA and Tau concentrations among the three groups. In summary, excitatory amino acids increased significantly after DHCA, and relative higher hematocrit attenuates this response.

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“…Excessive glutamate release is regarded as a trigger of neuronal cell damage during cerebral ischemia [20]. To examine whether KGKR acts directly on pre-synaptic glutamatergic neurons, we measured the effect of KGKR on glutamate release in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Ameliorating effects of Kangen-karyu on neuronal damage in rats subjected to repeated cerebral ischemia

Kaneko

Enoki

et al. 2010

J Nat Med

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We previously reported that 21-day (14-day pre-ischemic and 7-day post-ischemic) treatment with Kangen-karyu (KGKR) improved spatial memory impairment and hippocampal neuronal death induced by repeated cerebral ischemia (2 x 10-min, 1-h interval) in rats. In the present study, we examined the effect of single and 14-day pre-ischemic KGKR treatment on neuronal damage in the same repeated cerebral ischemia model. Additionally, to determine the mechanisms of neuroprotection by KGKR at glutamatergic neurons, we examined the effects of KGKR on glutamate release induced by repeated cerebral ischemia in vivo, and on cell damage induced by both glutamate and kainate in primary cultured hippocampal neurons in vitro. The 14-day pre-ischemic KGKR (300 mg/kg, oral administration (p.o.)) treatment reduced neuronal damage and astrocyte expression induced by repeated cerebral ischemia. No effect was observed after single pre-ischemic KGKR treatment. Both single and 14-day KGKR treatment decreased glutamate release in the hippocampal CA1 region in intact rats; however, neither pre-ischemic KGKR treatment altered glutamate release during cerebral ischemia. In vitro, KGKR (100-1000 microg/mL) dose-dependently suppressed hippocampal neuronal damage induced by both glutamate (100 microM) and kainate (1 mM). These data suggest neuroprotection with KGKR requires continuous pre-ischemic treatment, and that the mechanisms of protection may be involved in inhibiting the glutamatergic receptors of the post-synaptic neurons.

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Ischemic Neuronal Damage

Cited by 124 publications

References 0 publications

Spatiotemporal characteristics of calcium dynamics in astrocytes

Spatiotemporal characteristics of calcium dynamics in astrocytes

Relative Higher Hematocrit Attenuates the Cerebral Excitatory Amino Acid Elevation Induced by Deep Hypothermic Circulatory Arrest in Rats

Ameliorating effects of Kangen-karyu on neuronal damage in rats subjected to repeated cerebral ischemia

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