von Cornelia Larissa Granz
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| [1.] Clg/Fragment 008 01 - Diskussion Zuletzt bearbeitet: 2014-05-10 18:18:16 Singulus | Clg, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 8, Zeilen: 1-4, 7-9 |
Quelle: Gorji 2001 Seite(n): 34, Zeilen: left col. 44-46 - right col. 1-7 |
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| No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the spread of SD probably involves the release and diffusion of the chemical mediators, most likely K+ and glutamate into the interstitial fluid. [...] Given the widespread potential signaling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation. | No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the spread of SD probably involves the release and diffusion of the chemical mediators, most likely K+ and glutamate into the interstitial fluid [440]. Given the widespread potential signaling capacities of Ca2+ waves [332], observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation [231,299].
[231] PE. Kunkler, R.P. Kraig, Calcium waves precede electrophysiological changes of spreading depression in hippocampal organ cultures, J. Neurosci. 18 (1998) 3416-3425. [299] M. Nedergaard, Direct signaling from astrocytes to neurons in cultures of mammalian brain cells, Science 263 (1994) 1768-1771. [332] V. Parpura, T.A. Basarsky, F. Liu, K. Jeftinija, S. Jeftinia, P.G. Haydon, Glutamate-mediated astrocyte-neuron signaling, Nature 369 (1994) 744-747. [440] A. Van Harreveld, Two mechanisms for spreading depression in the chicken retina, J. Neurobiol. 9 (1978) 419-431. |
Nothing is marked as a citation. Complements Clg/Fragment_008_04. |
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| [2.] Clg/Fragment 008 04 - Diskussion Zuletzt bearbeitet: 2014-05-10 23:40:14 Schumann | Clg, Fragment, Gesichtet, James et al 2001, SMWFragment, Schutzlevel sysop, Verschleierung |
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| Untersuchte Arbeit: Seite: 8, Zeilen: 4-7, 10-18 |
Quelle: James et al 2001 Seite(n): 267, Zeilen: box 1:left col. 21ff |
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| In the isolated chick retina, human neocortical tissue and cat brain, NMDA receptor antagonists block SD completely. By contrast, in rat hippocampus, glutamate and Ca2+ facilitate SD initiation, whereas NMDA antagonists and low Ca2+]o delay its onset but fail to block SD completely. Given the widespread potential signaling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation.
Both volume-activated ion channels and glial cells probably play important roles in the restoration of normal cellular homeostasis. The former are stimulated during cell swelling, and the latter provide spatial buffering that prevents increased levels of [K+]o and [Glu−]o during normal neuronal activity. However, they might also prolong SD: volume-activated ion channels release glutamate during SD; and although gliotoxins prolong SD, they also reduce glutamate efflux from glial cells. SD appears more difficult to evoke in brains of larger animals in which the ratio of glia to neurones tends to be higher, suggesting that glial cells are important for limiting SD activity. Such limiting forces might be greater in the more complexly folded human brain, and could explain the paucity of literature accounts of SD during neurosurgery. |
In the isolated chick retinad, human neocortical tissuee and cat brainf, NMDA receptor antagonists block SD completely. By contrast, in rat hippocampus, glutamate (and Ca2+) facilitates SD initiation, whereas NMDA antagonists (and low [Ca2+]o) delay its onset but fail to block SD completelyg–i.
Both volume-activated ion channelsj,k and glial cells probably play important roles in the restoration of normal cellular homeostasis. The former are stimulated during cell swelling, and the latter provide spatial buffering that prevents increased levels of [K+]o and [Glu−]o during normal neuronal activity. However, they might also prolong CSD: volume-activated ion channels release glutamate during CSD (Ref. l); and although gliotoxins prolong CSD (Ref. m), they also reduce glutamate efflux from glial cellsn. CSD and PID appear more difficult to evoke in brains of larger animals in which the ratio of glia to neurones tends to be higher, suggesting that glial cells are important for limiting CSD activityo. Such limiting forces might be greater in the more complexly folded human brain, and could explain the paucity of literature accounts of CSD during neurosurgery. |
Bereft of all its original literary references; nothing is marked as a citation. Is complemented by Clg/Fragment_008_01. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Singulus, Zeitstempel: 20140510182758