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21 gesichtete, geschützte Fragmente: Plagiat

[1.] Aeh/Fragment 006 17 - Diskussion
Bearbeitet: 30. April 2014, 06:07 PlagProf:-)
Erstellt: 30. April 2014, 00:52 (Hindemith)
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Somjen 2001, Verschleierung

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Quelle: Somjen 2001
Seite(n): 1066, 1067, Zeilen: 1066: r.col: last 3 lines; 1067: l.col: 1ff
The first paper on SD, titled "Spreading depression of activity in the cerebral cortex" appeared in 1944, written by a Brazilian neuroscientist, Aristides Leão, working at the Harvard laboratory. Leão wanted to study the electrocorticogram (ECoG) of experimental epilepsy in anesthetized rabbits, but he was distracted from his original goal by an unexpected flattening of the ongoing normal bioelectrical activity that took the place of the anticipated epileptiform field potentials. The silencing of the ECoG trace crept slowly over the cortex, from one recording electrode pair resting on the cortical surface to the one beside it. According to Leão, SD and propagating focal seizures were related phenomena, generated by the same cellular elements, an inference later supported by others. The first, seminal paper on SD, titled “Spreading depression of activity in the cerebral cortex” (213) appeared in 1944, written by a young and unknown Brazilian inves-

[page 1067]

tigator, Aristides Leão, working at the Harvard laboratory of R. S. Morison. Leão wanted to study the cortical electrogram (ECoG) of experimental epilepsy in anesthetized rabbits, but he was distracted from his original goal by an unexpected silencing of the ongoing normal electrical activity that took the place of the anticipated seizure (Fig. 1). The flattening of the ECoG trace crept slowly over the cortex, from one recording electrode pair resting on the cortical surface to the one beside it. According to Leão, SD and propagating focal seizures were related phenomena, generated by the same cellular elements (213), an inference later supported by others (e.g., Ref. 428).


[...]

Anmerkungen

The source is indicated in the bibliographry, but no reference is made in the present context.

Sichter
(Hindemith), PlagProf:-)

[2.] Aeh/Fragment 015 03 - Diskussion
Bearbeitet: 30. April 2014, 00:05 Schumann
Erstellt: 29. April 2014, 23:56 (Hindemith)
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sheikh 2009, Verschleierung

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Quelle: Sheikh 2009
Seite(n): 14, Zeilen: 10-17
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.

Sichter
(Hindemith) Schumann

[3.] Aeh/Fragment 008 01 - Diskussion
Bearbeitet: 29. April 2014, 23:49 Schumann
Erstellt: 29. April 2014, 23:06 (Hindemith)
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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Seite(n): 8, 9, Zeilen: 8: 1-2; 9: figure
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.

Sichter
(Hindemith) Schumann

[4.] Aeh/Fragment 007 19 - Diskussion
Bearbeitet: 29. April 2014, 23:00 Schumann
Erstellt: 29. April 2014, 22:56 (Hindemith)
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sheikh 2009, Verschleierung

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Quelle: Sheikh 2009
Seite(n): 7, Zeilen: 16-22
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.

Sichter
(Hindemith) Schumann

[5.] Aeh/Fragment 017 06 - Diskussion
Bearbeitet: 29. April 2014, 22:36 Schumann
Erstellt: 29. April 2014, 22:29 (Hindemith)
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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Seite(n): 22, Zeilen: 7-19
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."

Sichter
(Hindemith) Schumann

[6.] Aeh/Fragment 019 19 - Diskussion
Bearbeitet: 29. April 2014, 22:32 Schumann
Erstellt: 29. April 2014, 22:18 (Hindemith)
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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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

[7.] Aeh/Fragment 020 01 - Diskussion
Bearbeitet: 29. April 2014, 22:26 Schumann
Erstellt: 29. April 2014, 22:13 (Hindemith)
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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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

[8.] Aeh/Fragment 013 01 - Diskussion
Bearbeitet: 29. April 2014, 22:23 Schumann
Erstellt: 29. April 2014, 21:45 (Hindemith)
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung, Wernsmann et al 2006

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A glass electrode filled with 2 m KCl was fixed in a special holder connected with plastic tube to a pressure injector and the tip inserted into the temporal neocortical slices (layer III). A high-pressure pulse was applied to inject in the tissue an amount of K+ sufficient to induce CSD (tip diameter, 2 μm; injection pressure, 0.5–1.0 bar applied for 200–300 ms, two separate injections, 1–3 nL per pulse, 2–5 mm apart from nearby recording electrodes). CSD were evaluated with respect to their amplitudes, duration and velocity rates. Duration of DC potential fluctuation width was measured at its half-maximal amplitude. A glass electrode filled with 2 m KCl was fixed in a special holder connected with plastic tube to a pressure injector and the tip inserted into the temporal neocortical slices (layer I–II) and hippocampal tissues (CA1 area). A high-pressure pulse was applied to inject in the tissue an amount of K+ sufficient to induce SD (tip diameter, 2 μm; injection pressure, 0.5–1.0 bar applied for 200–300 ms, up to two separate injections, 1–3 nL per pulse, 2–5 mm apart from nearby recording electrodes). SD were evaluated with respect to their amplitudes, duration and velocity rates. Duration of DC potential fluctuation width was measured at its half-maximal amplitude.
Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[9.] Aeh/Fragment 012 08 - Diskussion
Bearbeitet: 29. April 2014, 22:19 Schumann
Erstellt: 29. April 2014, 21:30 (Hindemith)
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wernsmann et al 2006

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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. Slices were stored at 28 °C in artificial cerebrospinal fluid (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 given.

On the one hand this is the description of an experimental procedure where the variation of wordings is neither easy nor desirable. On the other hand mentioning the study where this procedure has been employed in exactly the same way before would give credit to that study and would aid the interpretation of results.

Sichter
(Hindemith) Schumann

[10.] Aeh/Fragment 006 05 - Diskussion
Bearbeitet: 29. April 2014, 22:12 Schumann
Erstellt: 29. April 2014, 20:54 (Hindemith)
Aeh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Smith et al 2006, Verschleierung

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It was first induced by applying a brief tetanus of faradic stimulation to the rabbit cortex (Leao, 1944; Bures et al., 1974). Mechanical stimulation, for example, by stroking of the cortical surface with a blunt instrument, a falling weight or even lightly tapping the cortex also initiates SD (Lea˜o [sic], 1944). More recent studies have achieved more reliable and reproducible induction of SD by rapidly inserting and retracting hypodermic steel needles (Lambert et al., 1999; Ebersberger et al., 2001). [...] This model has been shown to be the most reliable stimulus leading to reproducible events on earlier occasions in both non-imaging and imaging studies (Bradley et al., 2001). In any case, changes in extracellular K+ concentration themselves might be involved in such pathophysiological processes in human brain tissue (Mayevsky et al., 1996; Nicholson and Sykova, 1998). SD appears to affect both the neuronal and the glial cells. The CSD phenomenon is exclusive to the central nervous system (CNS) and appears to involve both the neuronal and the glial cell populations. [...] CSD was first induced by applying a brief tetanus of faradic stimulation to the rabbit cortex (Leão, 1944; Bureš, Buresová & Krivánek, 1974). [...]

Mechanical stimulation, for example, by stroking of the cortical surface with a blunt instrument, a falling weight or even lightly tapping the cortex also evokes CSD (Leão, 1944; Zachar & Zacharová, 1963). More recent studies have achieved more reliable and reproducible induction of CSD by rapidly inserting and retracting hypodermic steel needles (Kaube & Goadsby, 1994; Lambert et al., 1999; Ebersberger et al., 2001), [...]

Of available methods KCl has thus proven to be the most reliable stimulus leading to reproducible events on earlier occasions in both non-imaging (Bureš et al., 1974, 1984; Lehmankühler & Richter, 1993; Smith et al., 1998, 2000; Read et al., 1999; Martins-Ferreira et al., 2000; Kuge et al., 2000) and imaging studies (Gardner-Medwin et al., 1994; Latour et al., 1994;Hasegawa et al., 1995; de Crespigny et al., 1996, 1998; James et al., 1999; Bockhorst et al., 2000; Kuge et al., 2000; Bradley et al., 2001, 2002). In any case, changes in extracellular K+ concentration ([K+])o themselves might be involved in such pathophysiological processes in human brain tissue (Mayevsky et al., 1996; Nicholson & Sykova´, 1998).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[11.] Aeh/Fragment 017 17 - Diskussion
Bearbeitet: 29. April 2014, 17:59 Singulus
Erstellt: 28. April 2014, 23:01 (Hindemith)
Aeh, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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It was postulated that the excitatory amino acid glutamate plays a role in the chain of events triggering SD (Bures et al., 1974). The neocortex releases excitatory amino acids including glutamate and aspartate, to the extracellular space during CSD (Van Harreveld and Kooiman, 1965). Subsequently it has been shown that the triggering of SD requires activation of the NMDA subtype of glutamate receptor in rat cerebral cortex (Bures et al., 1974), in chick retina (Seeling, 1993) and in human neocortical tissues (Gorji et al., 2001). Other glutamate subreceptor (AMPA, kainate and quisqualate) can induce SD but their initiation inhibited by [NMDA receptor antagonist (Lauritzen et al., 1988).]

Bures J., Buresova O., Krivanek J. In: The Mechanisms and Applications of Leao’s Spreading Depression of Electroencephalographic Activity, Academic Press, New York (1974).

Gorji A, Scheller D, Straub H, Tegtmeier F, Köhling R, Höhling JM, Tuxhorn I, Ebner A, Wolf P, Werner Panneck H, Oppel F, Speckmann EJ. Spreading depression in human neocortical slices. Brain Res. 2001;906:74-83.

Lauritzen M, Rice ME, Okada Y, Nicholson C. Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum. Brain Res. 1988; 475:317–327.

Seelig MS, Interrelationship of magnesium and estrogen in cardiovascular and bone disorders, eclampsia, migraine and premenstrual syndrome. J. Am. Coll. Nutr. 1993;12:442–458.

Van Harreveld A, Kooiman M. Amino acid release from the cerebral cortex during spreading depression and asphyxiation. J. Neurochem. 1965;12:431–439.

It was postulated that the excitatory amino acid glutamate plays a role in the chain of events triggering SD [442,443]. The brain cortex releases excitatory amino acids including glutamate and aspartate, to the extracellular space during CSD [447]. Subsequently it has been shown that the triggering of SD requires activation of the NMDA subtype of glutamate receptor in rat cerebral cortex [147,261], in chick retina [380] and in human neocortical tissues [149]. Other glutamate receptor subtypes (AMPA, kainate and quisqualate) can induce SD but their effects inhibited by NMDA receptor antagonist [241,383].

[147] N.A. Gorelova, V.I. Koroleva, T. Amemori, V. Pavlik, J. Bures, Ketamine blockade of cortical spreading depression in rats, Electroencephalogr. Clin. Neurophysiol. 66 (1987) 440-447.

[149] A. Gorji, D. Scheller, H. Straub, F. Tegtmeier, A. Ebnen, P. Wolf, H.W. Panneck, F. Oppel, E.-J. Speckmann, R. Kohling, J. Hohling, I. Tuxhorn, Spreading depression in neocortical human slices, Brain Res. 906 (2001) 74-83.

[241] M. Lauritzen, M.E. Rice, Y. Okada, C. Nicholson, Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum, Brain Res. 475 (1988) 317-327.

[261] R. Marrannes, R. Willems, E. De Prins, A. Wauquier, Evidence for a role of the N-metPyl-D-aspartate (NMDA) receptor in cortical spreading depression in the rat, Brain Res. 457 (1988) 226-240.

[380] M.S. Seelig, Interrelationship of magnesium and estrogen in cardiovascular and bone disorders, eclampsia, migraine and premenstrual syndrome, J. Am. Coll. Nutr. 12 (1993) 442-458.

[383] M.J. Sheardown, The triggering of spreading depression in the chicken retina: a pharmacological study, Brain Res. 607 (1993) 189-194.

[442] A. Van Harreveld, Compounds in brain extracts causing spreading depression of cerebral cortical activity and contraction of crustacean muscle, J. Neurochem. 3 (1959) 300-315.

[443] A. Van Harreveld, E. Fifkova, Glutamate release from the retina during spreading depression, J. Neurobiol. 2 (1970) 13-29.

[447] A. Van Harreveld, M. Kooiman, Amino acid release from the cerebral cortex during spreading depression and asphyxiation, J. Neurochem. 12 (1965) 431-439.

Anmerkungen

The source is not mentioned.

The correct Gorji et al. paper appears to have the title: "Spreading depression in human neocortical slices"; the other seems not to exist.

Sichter
(Hindemith) Singulus

[12.] Aeh/Fragment 018 01 - Diskussion
Bearbeitet: 29. April 2014, 17:38 Singulus
Erstellt: 28. April 2014, 22:35 (Hindemith)
Aeh, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Quelle: Gorji 2001
Seite(n): 38, Zeilen: l.col: 30ff
This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs (Ferrari et al., 1990). Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls (Martinez et al., 1993). Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM (Kaube et al., 2000). Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs (Nicolodi and Sicuteri, 1995). In addition, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats (Goadsby and Classey, 2000). The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents (Mitsikostas et al., 1989).

5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex (Edagawa et al., 1999). NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats (Kruger et al., 1999). Migraine patients have a greater cerebral 5-HT1A hypersensitivity and several anti-migraine agents exhibit marked 5-HT1A receptor activity (Leone et al., 1998).


Edagawa Y, Saito H, Abe K. Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex. Brain Res. 1999;827:225–228.

Ferrari MD, Odink J, Bos KD, Malessy MJ, Bruyn GW. Neuroexcitatory plasma amino acids are elevated in migraine. Neurology 1990; 40:1582–1586.

Goadsby PJ, Classey JD. Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow. Brain Res. 2000;875:119–124.

Kaube H, Herzog J, Kaufer T, Dichgans M, Diener HC. Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. Neurology 2000;55:139–141.

Kruger H, Heinemann U, Luhmann HJ. Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices. Neuroreport 1999;10:2651–2656.

Leone M, Attanasio A, Croci D, Ferraris A, D’Amico D, Grazzi L, Nespolo A,. Bussone G. 5- HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test. Neuroreport 1998;9:2605–2608.

Martinez F, Castillo J, Rodriguez JR, Leira R, Noya M. Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks. Cephalalgia 1993;13:89–93.

Mitsikostas DD, Sanchez del Rio M, Waeber C, Moskowitz MA, Cutrer F. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis. Pain 1998;76:239–248.

Nicolodi M, Sicuteri F. Exploration of NMDA receptors in migraine: therapeutic and theoretic implications. Int. J. Clin. Pharmacol. Res. 1995; 15:181–189.

This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs [125]. Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls [263]. Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM [205]. Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs [307]. Furthermore, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats [140]. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents [289].

As mentioned, migraineurs have a greater cerebral 5-HT1A hypersensitivity and several antimigraine agents exhibit marked 5-HT1A receptor activity [247,302]. 5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex [116]. NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats [228].


[116] Y. Edagawa, H. Saito, K. Abe, Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex, Brain Res. 827 (1999) 225-228.

[125] M.D. Ferrari, J. Odink, K.D. Bos, M.J. Malessy, G.W. Bruyn, Neuroexcitatory plasma amino acids are elevated in migraine, Neurology 40 (1990) 1582-1586.

[140] PJ. Goadsby, J.D. Classey, Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow, Brain Res. 875 (2000) 119-124.

[205] H. Kaube, J. Herzog, T. Kaufer, M. Dichgans, H.C. Diener, Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine, Neurology 55 (2000) 139-141.

[228] H. Kruger, U. Heinemann, H.J. Luhmann, Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices, Neuroreport 10 (1999) 2651-2656.

[247] M. Leone, A. Attanasio, D. Croci, A. Ferraris, D. D’Amico, L. Grazzi, A. Nespolo, G. Bussone, 5-HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test, Neuroreport 9 (1998) 2605-2608.

[263] F. Martinez, J. Castillo, J.R. Rodriguez, R. Leira, M. Noya, Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks, Cephalalgia 13 (1993) 89-93.

[289] D.D. Mitsikostas, M. SancPez del Rio, C. Waeber, M.A. Moskowitz, F.M. Cutrer, The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis, Pain 76 (1998) 239-248.

[302] A. Newman-Tancredi, C. Conte, C. Chaput, L. Verriele, V. Audinot- Bouchez, S. Lochon, G. Lavielle, M.J. Millan, Agonist activity of antimigraine drugs at recombinant human 5-HT1A receptors: potential implications for prophylactic and acute therapy, Naunyn Schmtrerbrrg’s ArcP. Pharmacol. 355 (1997) 682-688.

[307] M. Nicolodi, F. Sicuteri, Exploration of NMDA receptors in migraine: therapeutic and theoretic implications, Int. J. Clin. Pharmacol. Res. 15 (1995) 181-189.

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[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].


[...]

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SD is also 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.] 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 [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].
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[15.] Aeh/Fragment 007 02 - Diskussion
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SD appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression. A crucial manifestation of SD is a propagating negative potential with amplitude of 10–30 mV and duration of more than 30 sec, which may be preceded or succeeded by a positive fluctuation of variable amplitude and duration (Figure 1). Underlying this cellular depolarisation is a dramatic change in the distribution of micromilieu ions between extra- and intracellular compartments. Potassium and proton release from the cells, while sodium, calcium and chloride enter together with water causing cells to swell and the volume of the extracellular compartment to be decreased. SD is accompanied by an increase of glucose utilization and O2 consumption. Recovery of SD depends on energy metabolism.

SD has been studied in vivo and in vitro in brain slices and in retinal preparations under different experimental conditions. It has been also observed in human neocortical tissue in vitro and in human hippocampus as well as striatum and neocortex in vivo. SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoxia as well as hypoglycemia and changing the extracellular ionic concentrations by administration of solutions with increased K+, decreased NaCl or with the Cl of the latter replaced by certain other anions lower the threshold (Gorji, 2001).

It appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression [243]. A necessary manifestation of SD is a propagating extracellular negative potential with an amplitude of 10-30 mV and a duration of more than 0.5-1 min, which may be preceded or succeeded by a positive deflection of variable amplitude and duration. Underlying this neuro-glial depolarization is a dramatic change in the distribution of ions between extra- and intracellular spaces. K+ and H+ release from the cells, while Na+, Ca2+ and Cl- enter together with water [152,166,222] causing cells to swell and the volume of the extracellular compartment to be reduced. SD is accompanied by an increase of glucose utilization and O2 consumption [47,283]. Recovery of SD depends on energy metabolism [47].

This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under various experimental conditions [47]. It has been also observed in human neocortical tissue in vitro [16,17,149] and in human hippocampus as well as striatum [408] and neocortex [272] in vivo. [...]

SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold.

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The source is mentioned at the end, but it is not clear that the preceding two(!) paragraphs are taken from it.

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[16.] Aeh/Fragment 019 01 - Diskussion
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Magnesium is known to block the NMDA receptor. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium (Ramadan et al., 1999). Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls (James et al., 2000). Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients (Mauskop et al., 1995). However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters (Mauskop and Altura, 1998). It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues (Mody et al., 1987). Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats. On the other hand, SD affects magnesium metabolism in the central nervous system (van der Hel et al., 1998). The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals (Bohdanecky and Necina 1963).

Bohdanecky Z, Necina J. Course of some pharmacological tests in functionally decorticated animals. Physiol. Bohemoslov. 1963;12:55–61.

Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines. Clin. Neurosci. 1998;5:24–27.

Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. Clin. Sci. 1995;89:633–636.

Mody I, Lambert JD, Heinemann U. Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices. J. Neurophysiol. 1987;57:869– 888.

Ramadan NM, Halvorson H, Vande-Linde A, Levine SR, Helpern JA, Welch KM. Low brain magnesium in migraine. Headache 1989;29:590–593.

van der Hel WS, van den Bergh WM, Nicolay K, Tulleken KA, Dijkhuizen RM. Suppression of cortical spreading depressions after magnesium treatment in the rat. Neuroreport 1998;9:2179–2182.

Magnesium is known to block the NMDA receptor [271]. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium [348,455]. Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls [426]. Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients [270]. However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters [269]. It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues [16,291]. Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats [439]. On the other hand, SD affects magnesium metabolism in the central nervous system. The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals [35].

[16] M. Avoli, C. Drapeau, J. Louvel, R. Pumain, A. Olivier, J.G. Villemure, Epileptiform activity induced by low extracellular magnesium in the human cortex maintained in vitro, Ann. Neurol. 30 (1991) 589-596.

[35] Z. Bohdanecky, J. Necina, Course of some pharmacological tests in functionally decorticated animals, Physiol. Bohemoslov. 12 (1963) 55-61.

[269] A. Mauskop, B.M. Altura, Role of magnesium in the pathogenesis and treatment of migraines, Clin. Neurosci. 5 (1998) 24-27.

[270] A. Mauskop, B.T. Altura, R.Q. Cracco, B.M. Altura, Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study, Clin. Sci. 89 (1995) 633-636.

[271] M.L. Mayer, G.L. Westbrook, PB. Guthrie, Voltage-dependent block by Mg21 of NMDA responses in spinal cord neurones, Nature 309 (1984) 261-263.

[291] I. Mody, J.D. Lambert, U. Heinemann, Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices, J. NeuropPysiol. 57 (1987) 869-888.

[348] N.M. Ramadan, H. Halvorson, A. Vande-Linde, S.R. Levine, J.A. Helpern, K.M. Welch, Low brain magnesium in migraine, Headache 29 (1989) 590-593.

[426] J. Thomas, J.M. Millot, S. Sebille et al., Free and total magnesium in lymphocytes of migraine patients: effect of magnesium-rich mineral water intake, Clin. Chim. Acta 295 (2000) 63-75.

[439] W.S. van der Hel, W.M. van den Bergh, K. Nicolay, K.A. Tulleken, R.M. Dijkhuizen, Suppression of cortical spreading depressions after magnesium treatment in the rat, Neuroreport 9 (1998) 2179-2182.

[455] K.M. Welch, G.L. Barkley, N. Tepley, N.M. Ramadan, Central neurogenic mechanisms of migraine, Neurology 43 (1993) S21- S25.

Anmerkungen

The source is not mentioned.

Note: there is no entry "James et al., 2000" in the bibliography.

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[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). 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.

Among antecedents heralding the onset of SD that have been reported, are a slight increase of extracellular potassium ([K+]0), a small positive shift preceding the fast negative shift of the extracellular potential (ΔV0) (Marshall, 1959) and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Grafstein 1956; Rosenblueth and Garcia-Ramos, 1966; Ichijo and Ochs, 1970; Higashida et al., 1974; Somjen and Aitken, 1984; Haglund and Schwartzkroin, 1990; Herreras and Somjen, 1993a). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Grafstein, 1956; Morlock et al., 1964; Muiioz, 1970; 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.

[page 7097]

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; Dani et al., 1992; Finkbeiner, 1992). 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.

Anmerkungen

The source is not mentioned.

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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’,)

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Electrophysiological recordings

Simultaneous extracellular field potentials were recorded via two glass microelectrodes (150 mmol/L NaCl; 2 - 10 MΩ) positioned at approximately 5-10 mm intervals across the length of the slice in the third cortical layer (figure 2). The reference electrode and the connection to the microelectrode were symmetric Ag-Ag-KCl bridges. Field potentials were traced by an ink writer and recorded by a digital oscilloscope. Inter-electrode distances were measured with a calibrated eyepiece through the microscope.

Electrophysiological recordings

Simultaneous extracellular field potentials were recorded via four glass microelectrodes (150 mmol/L NaCl; 2 - 10 MΩ) positioned at approximately 2 - 3 mm intervals across the length of the slice in the third cortical layer. [...] The reference electrode and the connection to the microelectrode were symmetric Ag-Ag-KCl bridges. Field potentials were traced by an ink writer and recorded by a digital oscilloscope. Inter-electrode distances were measured with a calibrated eyepiece through the microscope.

Anmerkungen

The source is not mentioned.

In the abstract, on page 5 (8ff), one can read:
"Simultaneous field potential recordings of CSD were obtained from four microelectrodes placed 2-3 mm apart across coronal slices in the third layer of the neocortex."

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[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 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).

Grunze HC, Rainnie DG, Hasselmo ME, Barkai E, Hearn EF, McCarley RW, Greene RW. NMDA-dependent modulation of CA1 local circuit inhibition. J Neurosci 1996; 16: 2034-2043.

Wong BY, Prince DA. The lateral spread of ictal discharges in neocortical brain slices. Epilepsy Res 1990; 7: 29-39.

Wong RK, Miles R, Traub RD. Local circuit interactions in synchronization of cortical neurones. J Exp Biol 1984; 112: 169-178.

Inhibitory circuits may be particularly important to signal processing in cortical networks with pronounced recurrent excitatory interactions [53]. 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 [52] and disrupts the normal spread of lateral excitation [20].

20 Grunze HC, Rainnie DG, Hasselmo ME, Barkai E, Hearn EF, McCarley RW, Greene RW. NMDA-dependent modulation of CA1 local circuit inhibition. J Neurosci 1996; 16: 2034-2043

52 Wong BY, Prince DA. The lateral spread of ictal discharges in neocortical brain slices. Epilepsy Res 1990; 7: 29-39

53 Wong RK, Miles R, Traub RD. Local circuit interactions in synchronization of cortical neurones. J Exp Biol 1984; 112: 169-178

Anmerkungen

The source is not mentioned.

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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.

Mountcastle VB. The columnar organization of the neocortex. Brain 1997; 120: 701-722.

Cortical structures are organized to process information in a parallel manner via excitatory and inhibitory interactions within and between adjacent cortical modules [33]. Throughout the CNS, local circuit inhibition plays an integral role in both neuronal network processing and the regulation of the excitability of projection neurons.

33 Mountcastle VB. The columnar organization of the neocortex. Brain 1997; 120: 701-722

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