Angaben zur Quelle [Bearbeiten]
| Autor | Michael F. James, Justin M. Smith, Simon J. Boniface, Christopher L-H. Huang, Ronald A. Leslie |
| Titel | Cortical spreading depression and migraine: new insights from imaging? |
| Zeitschrift | Trends in Neurosciences |
| Datum | 1. May 2001 |
| Jahrgang | 24 |
| Nummer | 5 |
| Seiten | 266–271 |
| URL | http://leslie.medicine.dal.ca/Leslie/James%20et%20al%20TINS%20article.pdf |
Literaturverz. |
no |
| Fußnoten | yes |
| Fragmente | 2 |
| [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 |
|
|
|
| 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. |
Although the source is given (once inbetween) nothing has been marked as a citation. |
|
| [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 |
|
|
|
| Untersuchte Arbeit: Seite: 8, Zeilen: 4-7, 10-18 |
Quelle: James et al 2001 Seite(n): 267, Zeilen: box 1:left col. 21ff |
|---|---|
| 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. |
|