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Angaben zur Quelle [Bearbeiten]

Autor     Aziza El Harrak
Titel    Pharmacological investigation of spreading depression propagation in rat neocortical tissues
Ort    Münster
Jahr    2009
Anmerkung    Inaugural-Dissertation zur Erlangung des doctor medicinae dentium Der Medizinischen Fakultät der Westfälischen Wilhelms-Universität Münster
URL    http://miami1.uni-muenster.de/servlets/DocumentServlet?id=5045

Literaturverz.   

no
Fußnoten    no
Fragmente    5


Fragmente der Quelle:
[1.] Tmm/Fragment 011 04 - Diskussion
Zuletzt bearbeitet: 2014-04-25 09:18:07 Singulus
El Harrak 2009, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

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Untersuchte Arbeit:
Seite: 11, Zeilen: 4-29
Quelle: El Harrak 2009
Seite(n): 9, 10, Zeilen: 9: 14ff; 10: 1ff
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 than to the antecedent events. Among antecedents heralding the onset of SD that have been reported, are a slight increase of extracellular potassium, a small positive shift preceding the fast negative shift of the extracellular potential and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Higashida et al., 1974). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Higashida et al., 1974). Not all of these early signs are obligatory prodromals of the large, accelerating, regenerative depolarization that is typical of the process.

Even though the discharge of impulses is not required for the initiation or the propagation of SD, the impulse shower does regularly appear at its beginning. The mechanism that gives rise to the impulse discharge may well have a key role in the evolution of SD. The widely spread synchronization seems best explained by electrical continuity that could be provided by gap junctions. Effective communication by way of quasi-syncytial nets has been demonstrated in other systems, for example in the spread [of so-called calcium waves in cell cultures (Cornell- Bell et al., 1990).]

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. Among antecedents heralding the onset of SD that have been reported, are

[page 10]

a slight increase of extracellular potassium, a small positive shift preceding the fast negative shift of the extracellular potential and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Higashida et al., 1974). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Higashida et al., 1974). Not all of these early signs are obligatory prodromals of the large, accelerating, regenerative depolarization that is typical of the process.

Even though the discharge of impulses is not required for the initiation or the propagation of SD, the impulse shower does regularly appear at its beginning. The mechanism that gives rise to the impulse discharge may well have a key role in the evolution of SD. The widely spread synchronization seems best explained by electrical continuity that could be provided by gap junctions. Effective communication by way of quasi-syncytial nets has been demonstrated in other systems, for example in the spread of so-called calcium waves in cell cultures (Cornell-Bell et al., 1990).

Anmerkungen

The source is not mentioned.

For an explanation why the given references are to fairly old literature, refer to Tmm/Dublette/Fragment 011 04. There one can also see, what "AI’," actually is supposed to stand for.

Sichter
(Hindemith) Singulus

[2.] Tmm/Fragment 012 01 - Diskussion
Zuletzt bearbeitet: 2014-04-27 00:35:20 Hindemith
El Harrak 2009, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

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Quelle: El Harrak 2009
Seite(n): 10, 11, Zeilen: 10: 13ff - 11: 1ff
Patent gap junctions may provide a path not only for electric current and for ions but also for intracellular “second” messengers and other active ingredients in cytosol. SD has frequently been interpreted as a diffusion-reaction process whose velocity of spread is governed by the rate of the reaction, which could involve the release of some substance from cells that then acted on the cell membrane of adjacent cells. As there are reasons for doubting a decisive role of either K or of glutamate, we are proposing an alternative hypothesis, involving the exchange of chemical signals not through the interstitial space but by way of gap junctions. The autocatalytic reaction so initiated would alter the membrane from the inside, instead of acting on receptors on the outside.

Cortical structures are organized to process information in a parallel manner via excitatory and inhibitory interactions within and between adjacent cortical modules (Mountcastle, 1997). Throughout the CNS, local circuit inhibition plays an integral role in both neuronal network processing and the regulation of the excitability of projection neurons. Inhibitory circuits may be particularly important to signal processing in cortical networks with pronounced recurrent excitatory interactions (Wong et al., 1984). This inhibition may limit the propagation of excitation and facilitate discharge synchronization of projection neurons by inducing a synchronous refractory period. Breakdown in the dynamic balance of inhibitory and excitatory interaction can lead to a functional disconnection (Wong and Prince, 1990) and disrupts the normal spread of lateral excitation (Grunze et al., 1996).

Patent gap junctions may provide a path not only for electric current and for ions but also for intracellular “second” messengers and other active ingredients in cytosol. SD has frequently been interpreted as a diffusion-reaction process whose velocity of spread is governed by the rate of the reaction, which could involve the release of some substance from cells that then acted on the cell membrane of adjacent cells. As there are reasons for doubting a decisive role of either K or of glutamate, we are proposing an alternative hypothesis, involving the exchange of chemical signals not through the interstitial space but by way of gap junctions. The autocatalytic reaction so initiated would alter the membrane from the inside, instead of acting on receptors on the outside.

Cortical structures are organized to process information in a parallel manner via excitatory and inhibitory interactions within and between adjacent cortical modules (Mountcastle, 1997). Throughout the CNS, local circuit inhibition plays an integral role in both neuronal network processing and the regulation of the excitability of projection neurons. Inhibitory circuits may

[page 11]

be particularly important to signal processing in cortical networks with pronounced recurrent excitatory interactions (Wong et al., 1984). This inhibition may limit the lateral spread of excitation and facilitate discharge synchronization of projection neurons by inducing a synchronous refractory period. Breakdown in the dynamic balance of inhibitory and excitatory interaction can lead to a functional disconnection (Wong and Prince, 1990) and disrupts the normal spread of lateral excitation (Grunze et al., 1996).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[3.] Tmm/Fragment 014 01 - Diskussion
Zuletzt bearbeitet: 2014-04-27 00:35:23 Hindemith
El Harrak 2009, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

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Seite(n): 12, Zeilen: 1ff
Material and methods

Adult rats (250–300 g) were decapitated under deep methohexital anaesthesia and the brains were rapidly removed to ice-cold (4 °C) artificial cerebrospinal fluid (ACSF). The cerebellum was removed and a cut was made to divide the two cerebral hemispheres. Combined amygdala-hippocampus–cortex slices containing the temporal cortex, the perirhinal cortex, the entorhinal cortex, the subiculum, the dentate gyrus, the hippocampus, as well as the amygdala (500 μm) were cut in a nearly horizontal plane. Up to two different slices from each side were collected in a preparation. Slices were stored at 28 °C in ACSF, which contained (in mm) NaCl, 124; KCl, 4; CaCl2, 1.0; NaH2PO4, 1.24; MgSO4, 1.3; NaHCO3, 26; glucose, 10 (pH 7.4), oxygenated with 95% O2 and 5% CO2 for > 1 h. After 30-min incubation, CaCl2 was elevated to 2.0 mmol/L. Slices were individually transferred to an interphase recording chamber, placed on a transparent membrane, illuminated from below and continuously perfused (1.5–2 mL/min) with carbogenated ACSF at 32 °C. A warmed, humified 95% O2 and 5% CO2 gas mixture was directed over the surface of the slices.

Material and methods

Slice preparation

Adult rats (250–300 g) were decapitated under deep methohexital anaesthesia and the brains were rapidly removed to ice-cold (4 °C) artificial cerebrospinal fluid (ACSF). The cerebellum was removed and a cut was made to divide the two cerebral hemispheres. Slices containing the temporal cortex, the perirhinal cortex, the entorhinal cortex, the subiculum, the dentate gyrus, the hippocampus, as well as the amygdala (500 μm) were cut in a nearly horizontal plane. Up to two different slices from each side were collected in a preparation. Slices were stored at 28 °C in ACSF, which contained (in mm) NaCl, 124; KCl, 4; CaCl2, 1.0; NaH2PO4, 1.24; MgSO4, 1.3; NaHCO3, 26; glucose, 10 (pH 7.4), oxygenated with 95% O2 and 5% CO2 for > 1 h. After 30-min incubation, CaCl2 was elevated to 2.0 mmol/L. Slices were individually transferred to an interphase recording chamber, placed on a transparent membrane, illuminated from below and continuously perfused (1.5–2 mL/min) with carbogenated ACSF at 32 °C. A warmed, humified 95% O2 and 5% CO2 gas mixture was directed over the surface of the slices.

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[4.] Tmm/Fragment 015 19 - Diskussion
Zuletzt bearbeitet: 2014-04-28 19:32:57 Singulus
El Harrak 2009, Fragment, KeineWertung, SMWFragment, Schutzlevel, Tmm, ZuSichten

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Seite: 15, Zeilen: 19-23, 26-27
Quelle: El Harrak 2009
Seite(n): 13, Zeilen: 8ff
Experimental procedure

After minimum 30 min incubation, SD was induced by KCl application in temporal cortex. After another 15 min, several compounds were applied to the entorhinal cortex. Compounds applied were: DL-2-Amino-5-phosphonovaleric acid (APV; 50 μmol/L), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μmol/L), N-Methyl-D-Aspartat (NMDA; 10 μmol/L) bicuculline (10 μmol/L), 4-aminopyridine (4-AP; 20 μmol/L), and WIN 55212-2 (5 μmol/L). NMDA, APV, CNQX, bicuculline also applied in accompanied with induction of LTP in the neocortex. The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3 [μM, 0.5–2 bar; 500–800 ms, 3–5 nl).]

Experimental procedure

After minimum 30 min incubation, CSD was induced by KCl application. After another 15 min, several compounds were applied to small areas of cortex between the two middle electrodes of the four-channel array. Compounds applied were: DL-2-Amino-5- phosphonovaleric acid (APV; 50 μmol/L), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μmol/L), bicuculline (10 μmol/L), SKF 81297 (25 μmol/L), and quinpirole (20 μmol/L). The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3 μM, 0.5–2 bar; 500–800 ms, 3–5 nl).

Anmerkungen
Sichter
(Singulus)

[5.] Tmm/Fragment 016 01 - Diskussion
Zuletzt bearbeitet: 2014-04-27 00:35:27 Hindemith
El Harrak 2009, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

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Seite(n): 13, Zeilen: 13-17
[The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3] μM, 0.5–2 bar; 500–800 ms, 3–5 nl). Drugs were released through microelectrodes on to the surface of the slices. The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3 μM, 0.5–2 bar; 500–800 ms, 3–5 nl). Drugs were released through microelectrodes on to the surface of the slices.
Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

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