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Quelle: Granz 2009 Seite(n): 6, 8, Zeilen: 6: 18ff; 8: 10ff |
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| Changes in extracellular K+ concentration themselves might be involved in such pathophysiological processes in human brain tissue (Mayevsky et al., 1996; Nicholson & Sykova, 1998).
Other methods of SD induction are including: (1) application of the Na+-K+ ATP-ase inhibitor ouabain; (2) applications of the excitatory amino acids glutamate and aspartate; (3) administration of metabolic inhibitors such as NaCN and NaN that poison oxidative metabolism and NaF and iodoacetate that primarily interfere with glycolysis; (4) local cooling may initiate SD by depressing energy metabolism below a critical level but has proven an irreproducible experimental method. Furthermore, cooling itself raises the threshold for electrically or mechanically induced SD; (5) there are isolated reports of high-frequency electrical stimulation combined with the administration of pharmacological agents producing SD (Smith et al., 2006). 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. SD and neurological disorders Processes similar to SD phenomenon in animal cortex are thought to occur in different neurological disorders in humans. These conditions are migraine with aura, brain trauma, ischemia/infarction, brain haemorrhage, epilepsy, and transient global amnesia (Gorji, 2001). |
In any case, changes in extracellular K+ concentration themselves might be involved in such pathophysiological processes in human brain tissue (Mayevsky et al., 1996; Nicholson & Sykova, 1998).
Other methods of SD induction are including: (1) metabolic inhibitors such as NaCN and NaN that poison oxidative metabolism and NaF and iodoacetate that primarily interfere with glycolysis; (2) the Na+-K+ ATP-ase inhibitor ouabain has also been used in cortical brain slices; (3) applications of the excitatory amino acids glutamate and aspartate may elicit SD ; (4) local cooling may initiate SD by depressing energy metabolism below a critical level but has proven an irreproducible experimental method. Furthermore, cooling itself raises the threshold for electrically or mechanically induced SD.; (5) there are isolated reports of high-frequency electrical stimulation combined with the administration of pharmacological agents producing SD (Smith et al., 2006). [page 8] 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. 1. Clinical relevance of SD Processes similar to SD in animal cortex are thought to take place in a number of neuropathological conditions in humans. These conditions include migraine with aura, brain trauma, ischemia/ infarction, epilepsy, hemorrhage and transient global amnesia (see Gorji, 2001 for a recent review on clinical aspects of SD). |
The source is not mentioned. |
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