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Reconsolidation: Propagation of spreading depression between the neocortex and the hippocampus: the barrier of the entorhinal cortex

von Dr. Tanja Martens-Mantai

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[1.] Tmm/Fragment 009 01 - Diskussion
Zuletzt bearbeitet: 2014-04-28 15:49:17 Schumann
Fragment, Gesichtet, Granz 2009, SMWFragment, Schutzlevel sysop, Tmm, Verschleierung

Typus
Verschleierung
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 9, Zeilen: 1ff (complete)
Quelle: Granz 2009
Seite(n): 10, 11, 12, Zeilen: 10: 1-3, 11: 1-16, 12: 15-22
[However, it is believed that when SD] repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade (Somjen et al., 1990). The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating of SD in oxygen/glucose-deprived (ischemic) tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic areas increase in opacity (Obeidat and Andrew, 1998).

C) SD and epilepsy: SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, blocking of K+ channels, e.g., by 4-aminopyridine, activation of NMDA receptors, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of T-type Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for initiation of both epileptiform burst discharges and SD in experimental animal models (Gorji, 2001). By all abovementioned 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 (Koroleva and Bures, 1982). Penetration of cortical SD into epileptic foci established in different models 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 (Koroleva and Bures, 1982). SD was observed in association with epilepsy in patients suffering from brain vascular disorders (Fabricius et al., 2008). Regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in [migraine.]

b) SD and epilepsy

SD and epilepsy: regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in migraine.

[page 11]

SD is a well-known phenomenon in experimental epilepsy. 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 (Gorji, 2001). 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 (Koroleva and Bures, 1983). CSD penetration into epileptic foci established in different models 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 (Koroleva and Bures, 1983). SD was observed in association with epilepsy in patients suffering from brain vascular disorders (Fabricius et al., 2008).

[page 12]

However, it is believed that when SD repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade (Somjen et al., 1990). The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating SD in oxygen/glucose-deprived tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity (Obeidat and Andrew, 1998).

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Note that the sub- and superscripts have not made it into Tmm.

Sichter
(Hindemith) Schumann


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