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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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[1.] Tmm/Fragment 008 01 - Diskussion
Zuletzt bearbeitet: 2014-04-28 15:49:15 Schumann
Fragment, Gesichtet, Granz 2009, SMWFragment, Schutzlevel sysop, Tmm, Verschleierung

Typus
Verschleierung
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 8, Zeilen: 1ff (complete)
Quelle: Granz 2009
Seite(n): 11, 12, Zeilen: 11: 24ff - 12: 1ff
Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable (Olesen et al., 1986). The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core. There is a suggestion that the high potassium concentration in the ischemic focus initiates diffusion of K+ into the adjacent normally superfused cortex and triggers SD-like deflections propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard et al., 1986). Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is strong enough to support sufficiently intensive diffusion of active substances into the intact neocortex (Hossmann, 1996). A SD wave elicited from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 120 minutes period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3–4 h after the onset of focal ischemia (Koroleva et al., 1998). Such SD events are significantly longer than those occurring in normoxic neocortex and can be potentially harmful because they are accompanied by additional release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological or metabolic damage. Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable (Olesen et al., 1986). The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core. There is a suggestion that the high potassium concentration

[page 12]

in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard and Astrup, 1986). Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex (Hossmann, 1996). A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3–4 h after the onset of focal ischemia (Koroleva et al., 1998). Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological or metabolic damage.

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The source is not mentioned.

Sichter
(Hindemith) Schumann


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