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The effects of somatostatin on spreading depression in rat neocortical tissues

von Dr. Cornelia Larissa Granz

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Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
[1.] Clg/Fragment 007 01 - Diskussion
Zuletzt bearbeitet: 2014-05-10 18:50:46 Singulus
Clg, Fragment, Gesichtet, James et al 2001, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 1ff (complete page)
Quelle: James et al 2001
Seite(n): 267, 268, Zeilen: 267:box1, left col. 1-20; 268:left col. 4ff
SD probably starts with a cellular efflux of K+, leading to depolarization and a period of relative electrical silence. The subsequent energy-dependent restitution of ion gradients eventually restores normal neuronal activities. The ionic activity, however, results in a wave of neuronal depolarization propagating away from the elicitation site at a velocity of 3 mm/min. Because the depolarization-restoration process takes 1.5 min, the wave is only ~5 mm deep (James et al., 2001).

SD involves a temporary localized redistribution of different ions between intracellular and extracellular spaces. This ion redistribution is energy dependent. During eliciting of SD the concentration of extracellular K+ [K+]o, rapidly rises (up to 60mM), causing brief neuronal excitation then depolarization and a period of electrical silence during which DC potential at the brain surface falls. In tandem, [Na+]o and [Cl]o levels decrease as these ions enter cells. Consequently, water enters cells, the extracellular space is reduced, and cells swell. Ca2+ ions also move inwards, but slightly later than the outward movement of K+, suggesting that Ca2+ movements follow K+ fluxes. Additional negative ion species move outwards to maintain electrical balance, the excitatory neurotransmitter glutamate probably being the most important (Somjen et al., 2001).

[Page 267]

Cortical spreading depression (CSD) involves a temporary, but major, localized redistribution of ions between intracellular and extracellular compartments. This ion redistribution is energy dependenta, becoming clinically significant in ischaemia when brain metabolism is impaired. During CSD initiation the concentration of extracellular K+, [K+]o, rapidly rises, causing brief neuronal excitation then depolarization and a period of electrical silence during which the direct current (DC) potential at the brain surface falls. In tandem, [Na+]o and [Cl]o levels decrease as these ions enter cells. Consequently, water enters cells, the extracellular space is reduced, and cells swellb. Ca2+ ions also move inwards, but slightly later than the outward movement of K+, suggesting that Ca2+ movements follow K+ fluxes. Additional negative ion species move outwards to maintain electrical balance, the excitatory neurotransmitter glutamate probably being the most importantc.

[Page 268]

CSD probably starts with a cellular efflux of K+, leading to depolarization and a period of relative electrical silence (Box 1). The subsequent energy-dependent restitution of ion gradients eventually restores normal neuronal activity. The ionic activity, however, results in a wave of neuronal depolarization propagating away from the initiation site at a velocity of ~3 mm.min−1. Because the depolarization-restoration process takes ~1.5 min, the wave is only ~5 mm deep.

Anmerkungen

Although the source is given (once inbetween) nothing has been marked as a citation.

Sichter
(Graf Isolan) Singulus


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