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Reconsolidation: Propagation of spreading depression between the neocortex and the hippocampus: the barrier of the entorhinal cortex

von Dr. Tanja Martens-Mantai

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Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
[1.] Tmm/Fragment 010 01 - Diskussion
Zuletzt bearbeitet: 2014-04-28 15:49:20 Schumann
Fragment, Gesichtet, Granz 2009, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 10, Zeilen: 1ff (complete)
Quelle: Granz 2009
Seite(n): 8, 10, 12, Zeilen: 8: 1-7; 10: 3-11 12: 23-30
The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red. Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. A small but significant reduction in both of those was observed in cerebral hemisphere homolateral to the hypoperfused and hypometabolic areas (Bernardi et al., 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Olesen, 1986).

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarisations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non-NMDA receptor antagonist and by hypothermia (Mies et al., 1993; Mies et al., 1994).

Propagation of SD

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. 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.

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. 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.

[page 10]

The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red. Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. The small but significant reduction in both of those observed in cerebral hemisphere homolateral to the hypoperfused and hypometabolic areas (Bernardi et al., 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Olesen, 1986).

[page 12]

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non- NMDA receptor antagonist and by hypothermia (Mies et al., 1993; Mies et al., 1994).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann


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Letzte Bearbeitung dieser Seite: durch Benutzer:Schumann, Zeitstempel: 20140428155627

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