The effects of somatostatin on spreading depression in rat neocortical tissues
von Cornelia Larissa Granz
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| [1.] Clg/Fragment 011 01 - Diskussion Zuletzt bearbeitet: 2014-05-11 00:48:35 Schumann | Clg, Fragment, Gesichtet, Gorji 2005, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
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| 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 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 animals 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+ ATP-ase e.g. by ouabain, blocking of Ca2+ channels e.g. by NiCl2 , blocking of GABA receptors e.g. by picrotoxine are the common pathways for eliciting epileptiform burst discharges and SD in experimental models (Leao 1944A, Petsche et al. 1973, Traynelis and Dingledine 1988, Psarropoulou and Avoli 1992, Balestrino et al. 1999, Gorji et al. 2003A). 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, Gorji et al. 2000). 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 (Koroleva and Bures 1980, Bures et al. 1975). |
Nothing is marked as a citation. Can also be found in Quelle:Clg/Gorji 2001. |
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| [2.] Clg/Fragment 011 19 - Diskussion Zuletzt bearbeitet: 2014-05-11 00:49:34 Schumann | Clg, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 11, Zeilen: 19-33 |
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| The damage to cerebral tissue depends on a complex series of physiological responses and degradative cellular cascades involving a dynamic interplay among the various cells in the region of damaged tissue. Experimental studies of focal ischemic stroke in animals and human support the concept that there is a core of severe ischemia, the ‘ischemic core’ which is surrounded by a region of reduced perfusion, the ‘ischemic penumbra’. Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable (Olesen et al., 1986). The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core.
Olesen J (1986) Regional cerebral blood flow (rCBF) studies in migraine and epilepsy. Funct Neurol 1(4):369-74. |
The damage to cerebral tissue depends on a complex series of physiological responses and degradative cellular cascades involving a dynamic interplay among the various cells in the region of damaged tissue. Experimental studies of focal ischemic stroke in animals and human support the concept that there is a core of severe ischemia, the ‘ischemic core’, that is surrounded by a region of reduced perfusion, the ‘ischemic penumbra’. Within the ischemic core, failure of oxygen and glucose delivery leads to rapid depletion of energy stores and cell death. Central to the hypothesis of neuronal salvage is the concept of the ischemic penumbra. The penumbra is an area which metabolic capacity is suppressed but destruction is not yet inevitable [13,322]. The etiology of progressive cell injury and death in the penumbra zone has been clarified in some extent. Evidence suggests that SD plays a role in the ischemia–infarction tissue damage process. Excitotoxicity results from excessive release and impaired uptake of excitatory neurotransmitter glutamate. It is hypothesized that excessive amount of glutamate increases intracellular calcium preferentially via NMDA-receptor-mediated channels. A profound increase in extracellular potassium occurs in the ischemic core.
[13] J. Astrup, L. Symon, N.M. Branston, N.A. Lassen, Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia, Stroke 8 (1) (1977) 51-57. [321] J. Olesen, Regional cerebral blood flow (rCBF) studies in migraine and epilepsy, Funct. Neurol. 1 (1986) 369-374. [322] T.S. Olsen, Regional cerebral blood flow after occlusion of the middle cerebral artery, Acta Neurol. Scand. 73 (1986) 321-337. |
Nothing is marked as a citation. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Schumann, Zeitstempel: 20140511005003