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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 009 01 - Diskussion
Zuletzt bearbeitet: 2014-04-29 17:28:37 Singulus
Aeh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 9, Zeilen: 1-12
Quelle: Gorji 2001
Seite(n): 42, 43, Zeilen: 42: r.col: 47ff - 43: l.col: 1ff
[SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels,] e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models. By all aforementioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes. CSD penetration into the epileptic foci was established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals [sic] species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+ , blocking of Na+-K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models [22,149,150,243,337,344,433]. By all aforemen-

[page 43]

tioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes [150,217]. CSD penetration into epileptic foci established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy [50,215,217].


[...]

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[2.] Aeh/Fragment 009 14 - Diskussion
Zuletzt bearbeitet: 2014-04-29 16:45:58 Singulus
Aeh, Fragment, Gesichtet, Herreras et al 1994, SMWFragment, Schutzlevel sysop, Verschleierung

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Hindemith
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Untersuchte Arbeit:
Seite: 9, Zeilen: 14-25
Quelle: Herreras et al 1994
Seite(n): 7087, Zeilen: r.col: 8ff
Widely accepted hypotheses hold that the primary event responsible for both the initiation and the propagation of SD is the release of some substance from neuronal elements to the extracellular compartment, which initially excites and then depresses adjacent neurons. The slowness of diffusion of the mediator would account for the low velocity of SD propagation. Among the substances proposed to mediate SD propagation are potassium (Grafstein, 1963; Bures et al., 1974) and excitatory amino acids (Fabricius et al., 1993). There are, however, observations that are difficult to reconcile with either of these two propositions.

SD had been interpreted as a composite process or a sequence of several linked events. To solve its genesis, a most important question concerns identification of the very first step in the chain reaction. In the extant literature, however, generally more attention has been given to the major depolarization and the attending extracellular potential shift (AI’,) [sic] than to the antecedent events.

Widely accepted hypotheses hold that the primary event responsible for both the initiation and the propagation of SD is the release of some substance from neuronal elements to the extracellular compartment, which initially excites and then depresses adjacent neurons. The slowness of diffusion of the mediator would account for the low velocity of SD propagation. Among the substances proposed to mediate SD propagation are potassium (Grafstein, 1956; Brinley et al., 1960; BureS and Kiivanek, 1960) and excitatory amino acids (Van Harreveld, 1959; SiesjG and Bengtsson, 1989; Fabricius et al., 1993). There are, however, observations that are difficult to reconcile with either of these two propositions (Lehmenkiihler, 1990; Herreras and Somjen, 1993a,b; see also Discussion).

SD had been interpreted as a composite process or a sequence of several linked events. To solve its genesis, a most important question concerns identification of the very first step in the chain reaction. In the extant literature, however, generally more attention has been given to the major depolarization and the attending extracellular potential shift (ΔV0) than to the antecedent events.

Anmerkungen

The source is not mentioned.

Note, if one takes the online available version of the source and copies (ΔV0) and then pastes that expression, one obtains: (AI’,)

Sichter
(Hindemith) Singulus


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