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Pharmacological investigation of spreading depression propagation in rat neocortical tissues

von Dr. Aziza El Harrak

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[1.] Aeh/Fragment 007 02 - Diskussion
Zuletzt bearbeitet: 2014-04-29 16:59:21 Singulus
Aeh, BauernOpfer, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop

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Untersuchte Arbeit:
Seite: 7, Zeilen: 2-18
Quelle: Gorji 2001
Seite(n): 34, Zeilen: l.col: 7ff
SD appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression. A crucial manifestation of SD is a propagating negative potential with amplitude of 10–30 mV and duration of more than 30 sec, which may be preceded or succeeded by a positive fluctuation of variable amplitude and duration (Figure 1). Underlying this cellular depolarisation is a dramatic change in the distribution of micromilieu ions between extra- and intracellular compartments. Potassium and proton release from the cells, while sodium, calcium and chloride enter together with water causing cells to swell and the volume of the extracellular compartment to be decreased. SD is accompanied by an increase of glucose utilization and O2 consumption. Recovery of SD depends on energy metabolism.

SD has been studied in vivo and in vitro in brain slices and in retinal preparations under different experimental conditions. It has been also observed in human neocortical tissue in vitro and in human hippocampus as well as striatum and neocortex in vivo. SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoxia as well as hypoglycemia and changing the extracellular ionic concentrations by administration of solutions with increased K+, decreased NaCl or with the Cl of the latter replaced by certain other anions lower the threshold (Gorji, 2001).

It appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression [243]. A necessary manifestation of SD is a propagating extracellular negative potential with an amplitude of 10-30 mV and a duration of more than 0.5-1 min, which may be preceded or succeeded by a positive deflection of variable amplitude and duration. Underlying this neuro-glial depolarization is a dramatic change in the distribution of ions between extra- and intracellular spaces. K+ and H+ release from the cells, while Na+, Ca2+ and Cl- enter together with water [152,166,222] causing cells to swell and the volume of the extracellular compartment to be reduced. SD is accompanied by an increase of glucose utilization and O2 consumption [47,283]. Recovery of SD depends on energy metabolism [47].

This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under various experimental conditions [47]. It has been also observed in human neocortical tissue in vitro [16,17,149] and in human hippocampus as well as striatum [408] and neocortex [272] in vivo. [...]

SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold.

Anmerkungen

The source is mentioned at the end, but it is not clear that the preceding two(!) paragraphs are taken from it.

Sichter
(Hindemith) Singulus

[2.] Aeh/Fragment 007 19 - Diskussion
Zuletzt bearbeitet: 2014-04-29 23:00:43 Schumann
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sheikh 2009, Verschleierung

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Seite: 7, Zeilen: 19-25
Quelle: Sheikh 2009
Seite(n): 7, Zeilen: 16-22
There is sufficient evidence to admit the SD plays an important role in different neurological disorders (Gorji, 2001; Somjen, 2001). Subdural recordings in patients demonstrated that SD is critically involved in various disorders associated with acute neuronal injury including traumatic and spontaneous intracerebral haemorrhage (Strong et al., 2002; Fabricius et al., 2008) as well as subarachnoid haemorrhage and ischaemic stroke and contribute to tissue damage. Furthermore, propagation of a SD-like phenomenon in human neocortical tissues has been shown to generate aura symptoms in migrainous patients (Hadjikhani et al. 2001). There is sufficient evidence to admit the SD plays an important role in different neurological disorders (Gorji, 2000). Subdural recordings in patients demonstrated that SD is critically involved in various disorders associated with acute neuronal injury including traumatic and spontaneous intracerebral haemorrhage (Strong et al., 2002; Fabricius et al., 2006) as well as subarachnoid haemorrhage and ischaemic stroke (Dreier et al., 2006) and contribute to tissue damage. Furthermore, propagation of a SD-like phenomenon in human neocortical tissues has been shown to generate aura symptoms in migrainous patients (Hadjikhani et al. 2001).
Anmerkungen

The source is not mentioned.

Some of the literature given is different.

Sichter
(Hindemith) Schumann


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