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Angaben zur Quelle [Bearbeiten]

Autor     Khalil Sheikh
Titel    Spreading depression triggers ictal activity in disinhibited hippocampal slices
Ort    Münster
Jahr    2009
Anmerkung    Inaugural-Dissertation zur Erlangung des doctor medicinae der Medizinischen Fakultät der Westfälischen Wilhelms-Universität Münster, Tag der mündlichen Prüfung: 13.01.2009, Online publication: 05.02.2009
URL    http://miami1.uni-muenster.de/servlets/DocumentServlet?id=4626 , http://d-nb.info/992877040/34

Literaturverz.   

no
Fußnoten    no
Fragmente    6


Fragmente der Quelle:
[1.] 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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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.

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[2.] Aeh/Fragment 008 01 - Diskussion
Zuletzt bearbeitet: 2014-04-29 23:49:12 Schumann
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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Although interrelation of SD and epilepsy has been considered for a long time, the possible pathophysiological role of SD in epilepsy needs to be elucidated.

08 diss Aeh.png

Figure 1. Vertical propagation of a negative DC-potential wave after injection of KCl in a neocortical slice. Injection of KCl solution (3 M) via a microelectrode elicited spreading depression-like fluctuation during superfusion with artificial cerebrospinal fluid. Injecting and recording electrodes arranged as shown. Voltage variations were recorded simultaneously by four electrodes (DC1–DC4) which set apart by 1 mm (Adopted from Gorji et al., 2001).

Although interrelation of SD and epilepsy has been considered for a long time, the possible pathophysiological role of SD in epilepsy needs to be elucidated.

08 source Aeh.png

Fig. 1. Propagation of a negative DC-potential wave after injection of KCl in a neocortical slice. Injection of KCl solution (3 M) via a microelectrode elicited spreading depression-like fluctuation during superfusion with artificial cerebrospinal fluid. Injecting and recording electrodes arranged as shown. Voltage variations were recorded simultaneously by four electrodes (DC1–DC4) which set apart by 1 mm.

Anmerkungen

The copied text starts on the previous page: Aeh/Fragment_007_19.

Note that in Gorji et al., (2001) there is a very similar but slightly different figure with a slightly different figure caption.

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[3.] Aeh/Fragment 015 03 - Diskussion
Zuletzt bearbeitet: 2014-04-30 00:05:31 Schumann
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Application of KCl in to neocortical slices elicited fluctuations of the DC potentials consisting of initially negative shifts, followed by positive waves. The triggered wave propagated first the nearby electrode, and a few seconds later the other electrode located parallel to this electrode. The amplitude and duration of negative DC deflections were 13.6 ± 0.8 mV and 102 ± 13.1 seconds, respectively, in the first electrode. The amplitude and duration of CSD recorded by the second electrode was 11.5 ± 0.6 mV and 93 ± 10.3 seconds, respectively. The velocity of SD propagation was determined by dividing the distance between two microelectrodes by the interval of DC potential shift appearances. The velocity of vertical propagation of DC fluctuation was 3.6 ± 0.2 mm/min. Application of KCl into hippocampal slices elicited deflections of the DC potentials consisting of initially negative shifts, followed by positive waves (Fig. 1A). The amplitude and duration of negative DC deflections were 12.6 ± 0.7 mV and 93 ± 12.4 seconds, respectively. The triggered wave propagated against the flow of the superfusate and reached first the nearby electrode, and a few seconds later the other electrode located closer to the inlet of superfusate in the chamber. The velocity of SD propagation was determined by dividing the distance between two microelectrodes by the interval of DC potential shift appearances. The velocity of vertical propagation of DC fluctuation was 3.3 ± 0.1 mm/min.
Anmerkungen

The source is not mentioned.

The text has been adapted to accomodate the different set-up and results.

Note that it seems that "The triggered wave propagated against the flow of the superfusate and reached first the nearby electrode" was shortened to "The triggered wave propagated first the nearby electrode", which is not grammatically correct. This could be seen as an indication, that indeed Aeh (2009) has taken text from Sheikh (2009) and not the other way round.

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[4.] Aeh/Fragment 017 06 - Diskussion
Zuletzt bearbeitet: 2014-04-29 22:36:15 Schumann
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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SD cellular correlate is a depolarization shift associated with complete breakdown of the membrane potential that is dependent on the asymmetric intra- and extracellular ion distribution and is maintained by the energy consuming work of membrane pumps. The ability of neurons to generate action potentials is lost during SD, which explains the spreading electrical silence accompanied SD under physiological conditions (Somjen 2001). In [sic] the other hand, epileptic activity is characterized by the paroxysmal depolarization shift, a hypersynchronous network event resulting from a giant excitatory postsynaptic potential. A paroxysmal depolarization shift is the correlate of. [sic] The EPSP is presumably the consequence of synchronous activation of recurrent excitatory pathways (Jonston and Brown, 1984). SD is accompanied by a very large increase in [K+]o. The increase in [K+]o is accompanied by a precipitous drop in [Cl-]o, [Na+]o, and [Ca2+]o. SD cellular correlate is a depolarization shift associated with complete breakdown of the membrane potential that is dependent on the asymmetric intra-/extracellular ion distribution and is maintained by the energy consuming work of membrane pumps. The ability of neurons to generate action potentials is lost during SD, which explains the spreading electrical silence (depression of electrocorticographic activity) accompanied SD under physiological conditions (Somjen 2001). In [sic] the other hand, epileptic activity is characterized by the paroxysmal depolarization shift, a hypersynchronous network event resulting from a giant excitatory postsynaptic potential. A paroxysmal depolarization shift is the correlate of. [sic] The EPSP is presumably the consequence of synchronous activation of recurrent excitatory pathways (Jonston and Brown, 1984). [...] SD is accompanied by a very large increase in [K+]o. The increase in [K+]o is accompanied by a precipitous drop in [Cl-]o, [Na+]o, and [Ca2+]o.
Anmerkungen

The source is not mentioned.

Note that also errors have been copied from the source: "In the other hand", The truncated sentence: "A paroxysmal depolarization shift is the correlate of."

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[5.] Aeh/Fragment 019 19 - Diskussion
Zuletzt bearbeitet: 2014-04-29 22:32:44 Schumann
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Increasing of potassium concentration may further impairs GABA mediated inhibition and leads to appearance of ictaform burst discharges. Higashima et al. (1996) have shown that activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in [particular that induced by 4AP application).] Increasing of potassium concentration may further impairs GABA mediated inhibition and leads to appearance of ictaform burst discharges. Higashima et al. (1996) have shown that

[Seite 24]

activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in particular that induced by 4AP application).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[6.] Aeh/Fragment 020 01 - Diskussion
Zuletzt bearbeitet: 2014-04-29 22:26:29 Schumann
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GABAergic inhibitory networks can also synchronize principal cells in the neocortex and hippocampus (Cobb et al. 1995). Higashima et al. (1996) have shown that activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in particular that induced by 4AP application). GABAergic inhibitory networks can also synchronize principal cells in the neocortex and hippocampus (Cobb et al. 1995). GABAergic inhibitory networks can also synchronize principal cells in the neocortex and hippocampus (Cobb et al. 1995). Higashima et al. (1996) have shown that activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in particular that induced by 4AP application). GABAergic inhibitory networks can also synchronize principal cells in the neocortex and hippocampus (Cobb et al. 1995).
Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

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