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26 gesichtete, geschützte Fragmente: Plagiat

[1.] Clg/Fragment 021 02 - Diskussion
Bearbeitet: 11. May 2014, 22:54 Schumann
Erstellt: 11. May 2014, 22:42 (Graf Isolan)
Berger et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 21, Zeilen: 2-7
Quelle: Berger et al 2008
Seite(n): 561, Zeilen: Figure 1: 12-20
Fig. 5: [...] (A) Tetanic stimulation

(Ten trains of four pulses; pulse duration 0.1 msec; interpulse interval 50 msec; intensity 5 V) produces a rapid and stable potentiation in the amplitude of the evoked field potentials, calculated as a percentage of baseline mean response amplitude. Open triangles, open square, and closed circles show the evoked fEPSP after application of somatostatin (500 nmol/l), and control, respectively. Arrow shows the time of tetanic stimulation, 60 min after [application of substances.]

Figure 1 [...] (B2) Tetanic stimulation (10 trains of four pulses, pulse duration 0.1 ms; interpulse interval 50 ms) produces a rapid and stable potentiation in the amplitude of fEPSP, calculated as a percentage of baseline mean response amplitude. Solid hexagons and open circles show the evoked fEPSP after induction of CSD and control, respectively. Arrow shows the time of tetanic stimulation, 45 min after KCl application and ACSF (control).
Anmerkungen

Nothing is marked as a citation.

Sichter
(Graf Isolan) Schumann

[2.] Clg/Fragment 010 00 - Diskussion
Bearbeitet: 11. May 2014, 22:41 Schumann
Erstellt: 11. May 2014, 22:16 (Hindemith)
Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sheikh 2009, Verschleierung

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Seite: 10, Zeilen: figure
Quelle: Sheikh 2009
Seite(n): 9, Zeilen: figure
10a diss Clg.png

Fig. 2: Above row: a schematic pattern of propagation of spreading depression in human brain. Lower row: Traces recorded from human tissues. Vertical propagation of spreading depression reveals a very slow velocity of DC-negative deflection.

10a source Clg.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

There is no source given for this chart. On the precious page one finds at the end of the paragraph: "(Fig. 2; Gorji, 2001)", which could be interpreted as a reference of the figure. However, in Gorji (2001) the figure cannot be found.

Sichter
(Hindemith) Schumann

[3.] Clg/Fragment 024 03 - Diskussion
Bearbeitet: 11. May 2014, 22:33 Schumann
Erstellt: 11. May 2014, 21:25 (Hindemith)
Clg, Fragment, Gesichtet, Matharu et al 2004, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 24, Zeilen: 3-8
Quelle: Matharu et al 2004
Seite(n): 489, 491, Zeilen: 489: l.col: 10-14; 491: r.col: 31-36
Somatostatin has been shown to block the release of numerous vasoactive peptides, including Calcitonin Gene-Related Peptide and vasoactive intestinal polypeptide e et al.(Fassler et al., 1990; Helyes, 2001). Neurons containing somatostatin are found in the regions of the central and peripheral nervous system involved in nociception, such as peripheral sensory fibres, dorsal horn of the spinal cord, trigeminal nucleus caudalis, periaqueductal gray and the hypothalamus (Schindler et al., 1997).

Fassler JE, O'Dorisio TM, Mekhjian HS, Gaginella TS (1990) Octreotide inhibits increases in shortcircuit current induced in rat colon by VIP, substance P, serotonin and aminophylline. Regul Pept 29(2-3):189-97.

Helyes Z, Pintér E, Németh J, Kéri G, Thán M, Oroszi G, Horváth A, Szolcsányi J (2001) Antiinflammatory effect of synthetic somatostatin analogues in the rat. Br J Pharmacol 134 (7):1571-9.

Schindler M, Sellers LA, Humphrey PP, Emson PC (1997)Immunohistochemical localization of the somatostatin SST2(A) receptor in the rat brain and spinal cord. Neuroscience. 76(1):225-40.

Somatostatin, an endogenously occurring 14–amino acid peptide, has been shown to inhibit the release of numerous vasoactive peptides, including CGRP19 and VIP.20

[page 491]

Neurons containing somatostatin are found in the regions of the central and peripheral nervous system involved in nociception, such as peripheral sensory fibers, dorsal horn of the spinal cord, trigeminal nucleus caudalis, periaqueductal gray, and the hypothalamus.31,32


19. Helyes Z, Pinter E, Nemeth J, et al. Anti-inflammatory effect of synthetic somatostatin analogues in the rat. Br J Pharmacol 2001;134:1571–1579.

20. Fassler JE, O’Dorisio TM, Mekhjian HS, Gaginella TS. Octreotide inhibits increases in short-circuit current induced in rat colon by VIP, substance P, serotonin and aminophylline. Regul Pept 1990;29:189 –197.

31. Krisch B. Hypothalamic and extrahypothalamic distribution of somatostatin-immunoreactive elements in the rat brain. Cell Tissue Res 1978;195:499 –513.

32. Schindler M, Holloway S, Hathway G, et al. Identification of somatostatin sst2(a) receptor expressing neurones in central regions involved in nociception. Brain Res 1998;798:25–35.

Anmerkungen

Also the passages after the here documented passage can be found in the source, but the match seems to be somewhat better with another paper by the same author, see Clg/Fragment_024_08.

The source is given further down at the end of the paragraph but without indication that the whole paragraph is taken from it including several references to the literature.

Sichter
(Hindemith) Schumann

[4.] Clg/Fragment 023 08 - Diskussion
Bearbeitet: 11. May 2014, 22:25 Schumann
Erstellt: 11. May 2014, 21:35 (Hindemith)
Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung, Vezzani and Hoyer 1999

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Quelle: Vezzani and Hoyer 1999
Seite(n): 3767, Zeilen: r.col: 21-31
Regional differences in the concentration of somatostatin and its receptors have been found in the CNS, with the highest levels in the hypothalamus, cortex and limbic areas (Epelbaum, 1986; Thoss et al., 1997). The demonstration of a neuronal, Ca2+- and tetrodotoxindependent release of somatostatin (Iversen et al., 1978; Lee and Iversen 1981; Vezzani et al., 1993), its coexistence in neurons with classical neurotransmitters (Hokfelt, 1991) and its ability to affect neuronal activity and ionic currents (Scharfman, 1993) suggest that this neuropeptide has neurotransmitter and/or neuromodulator activities in the CNS. Regional differences in the concentration of SRIF and its receptors have been found in the CNS, with the highest levels in the hypothalamus, cortex and limbic areas (Epelbaum, 1986; Thoss et al, 1995, 1996a,b, 1997).

The demonstration of a neuronal, Ca2+- and tetrodotoxindependent release of SRIF (Iversen et al., 1978; Lee & Iversen, 1981; Arancibia et al., 1984; Vezzani et al., 1992, 1993), its coexistence in neurons with classical neurotransmitters (Epelbaum, 1986; Hokfelt, 1991) and its ability to affect neuronal activity and ionic currents (see Scharfman, 1993) suggest that this neuropeptide has neurotransmitter and/or neuromodulator activities in the CNS.

Anmerkungen

The source is not given here.

Sichter
(Hindemith) Schumann

[5.] Clg/Fragment 023 22 - Diskussion
Bearbeitet: 11. May 2014, 22:19 Schumann
Erstellt: 11. May 2014, 22:00 (Hindemith)
BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Vezzani and Hoyer 1999

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Untersuchte Arbeit:
Seite: 23, Zeilen: 22-31
Quelle: Vezzani and Hoyer 1999
Seite(n): 3768, 3773, Zeilen: 3768: l.col: 3-16; 3773: r.col: 13-19
1. The peptide is preferentially released during high-frequency neuronal activities (Bartfai et al., 1988; Hokfelt 1991; Vezzani et al., 1993). 2. Marked changes in the expression of somatostatin mRNA, the levels of the peptide and its receptors occur after experimentally induced epileptiform burst discharges (Pitkanen et al., 1986; Sloviter 1987; Marksteiner and Sperk 1988; Pérez et al., 1995; Piwko et al., 1996; Schwarzer et al., 1996) and in human epileptic tissue obtained during epilepsy surgery (Perlin et al., 1987; Nagaki et al., 1988; de Lanerolle et al.,. 1989; Deutch et al., 1991; Spencer and Spencer 1994). 3. Intracerebral injections of somatostatin affect seizures and epileptogenesis in experimental animals (Perlin et al., 1987; Mazarati and Telegdy 1992; Monno et al., 1993; Piwko et al., 1996). The data indicate association between somatostatin and epilepsy suggest that peptidergic systems may be an interesting target for pharmacological at[tempts to control pathological hyperactivity in neurons, pointing out new directions for the development of anticonvulsant treatments (Vezzani and Hoyer, 1999).] (i) The peptide is preferentially released from neurons under conditions of elevated activity (i.e. bursting or highfrequency neuronal activation, Bartfai et al., 1988; Hokfelt, 1991; Vezzani et al., 1993), e.g. during seizures. (ii) Marked changes in the expression of SRIF mRNA, the levels of the peptide and its receptors occur after experimentally induced seizures (Pitkanen et al., 1986; Sloviter, 1987; Marksteiner & Sperk, 1988; Perez et al., 1995; Piwko et al., 1996; for review see Schwarzer et al., 1996) and in human epileptic tissue (Perlin et al., 1987; Nagaki et al., 1988; de Lanerolle et al., 1989; Deutch et al., 1991; Spencer & Spencer, 1994). (iii) Intracerebral injections of SRIF, its analogues or SRIF-specific antibodies affect seizures and epileptogenesis in rats (Perlin et al., 1987; Vezzani et al., 1991; Mazarati & Telegdy, 1992; Monno et al., 1993; Piwko et al., 1996).

[page 3773]

Finally, although pharmacological evidence is still scarce because we lacked highly selective SRIF receptor ligands (Hoyer et al., 1995b; Humphrey et al., 1998) that only recently became available (Rohrer et al., 1998), it suggests that peptidergic systems may be an interesting target for pharmacological attempts to control pathological hyperactivity in neurons, pointing out new directions for the development of anticonvulsant treatments.

Anmerkungen

The source is given in the end, but as many other references are given in the here documented passage, the reader would never guess that the entire passage is taken from that source.

Also: quotations are not marked as such.

Sichter
(Hindemith) Schumann

[6.] Clg/Fragment 025 12 - Diskussion
Bearbeitet: 11. May 2014, 19:54 Schumann
Erstellt: 9. May 2014, 21:43 (Graf Isolan)
Baratta et al 2002, BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop

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Seite: 25, Zeilen: 12-30
Quelle: Baratta et al 2002
Seite(n): 3078, 3082, 3084, Zeilen: 3078:right col. 20-28; 3082:right col. 31-36; 3084:right col. 13-23.25-29.42-46
In hippocampal CA1 area,

somatostatin activates postsynaptic K+ currents in pyramidal neurons (Moore et al., 1988; Schweitzer et al., 1998) to hyperpolarize neurons away from their threshold for firing. Somatostatin inhibits glutamatergic excitatory postsynaptic currents at CA1 Schaeffer collateral synapses, while not affecting GABAergic inhibitory postsynaptic currents (Boehm and Betz 1997; Tallent and Siggins 1997). In CA3, somatostatin inhibits excitatory postsynaptic currents generated at associational/commissural synapses (Tallent and Siggins 1999). In line with our results, it has been reported that is released during high-frequency activation of somatostatin containing interneurons and acts to prevent LTP in lateral perforant pathway (Baratta et al., 2002). However some other studies have suggested that somatostatin facilitates LTP at some synapses in the hippocampus. An in vitro study in guinea pig demonstrated that SST augmented mossy fiber LTP in CA3 neurons (Matsuoka et al. 1991). In dentate, a previous in vivo study in rat suggested facilitation by SST of medial perforant path LTP (Nakata et al. 1996). Several inhibitory neuropeptides depress LTP in different brain structures. In vitro studies have shown nociceptin (Yu and Xie 1998), dynorphin (Terman et al. 1994) to depress LTP at lateral perforant pathway synapses. These peptides likely have a presynaptic site of action in inhibiting glutamate releases, although they could also act postsynaptically (Yu and Xie 1998). Neuropeptide Y inhibits N-type Ca2+ currents and Ca2+ transients in dentate granule cells (McQuiston et al. 1996); thus, like somatostatin, this is a possible mechanism through which this peptide could attenuate LTP.

[page 3078]

In CA1, SST activates postsynaptic K+ currents in pyramidal neurons (Moore et al. 1988; Schweitzer et al. 1998) to hyperpolarize neurons away from their threshold for firing. SST inhibits glutamatergic excitatory postsynaptic currents (EPSCs) at CA1 Schaeffer collateral synapses, while not affecting GABAergic inhibitory postsynaptic currents (Boehm and Betz 1997; Tallent and Siggins 1997). In CA3, SST inhibits EPSCs generated at associational/commissural synapses while not affecting mossy fiber EPSCs (Tallent and Siggins 1999).

[page 3082]

Previous studies have suggested that SST facilitates LTP at some synapses in the hippocampus. An in vitro study in guinea pig demonstrated that SST augmented mossy fiber LTP in CA3 neurons (Matsuoka et al. 1991). In dentate, a previous in vivo study in rat suggested facilitation by SST of medial perforant path LTP (Nakata et al. 1996).


[page 3084]

Multiple inhibitory neuropeptides depress dentate gyrus LTP. An in vivo study showed neuropeptide Y (NPY)-mediated inhibition of dentate LTP (Whittaker et al. 1999), whereas in vitro studies have shown nociceptin (Yu and Xie 1998), dynorphin (Terman et al. 1994), galanin, and cortistatin (unpublished observations) to depress LTP at LPP synapses. Some of these peptides robustly depress baseline perforant-path fEPSPs (i.e., dynorphin, nociceptin); these peptides likely have a presynaptic site of action in inhibiting glutamate releases, although they could also act postsynaptically (Yu and Xie 1998). [...] NPY inhibits N-type Ca2+ currents and Ca2+ transients in dentate granule cells (McQuiston et al. 1996); thus, like SST, this is a possible mechanism through which this peptide could attenuate LTP. [...]

Our results suggest SST is released during high-frequency activation of SST containing interneurons and acts to prevent LTP of LPP synapses. Seizure events have been shown to cause intense activation of SST/GABAergic hilar interneurons (Vezzani et al. 1996).

Anmerkungen

Nothing has been marked as a citation. The source is mentioned somewhere in between only once and only in passing.

Sichter
(Graf Isolan) Schumann

[7.] Clg/Fragment 006 01 - Diskussion
Bearbeitet: 11. May 2014, 19:41 Schumann
Erstellt: 10. May 2014, 22:07 (Hindemith)
BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Smith et al 2006

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Quelle: Smith et al 2006
Seite(n): 458, 459, 460, Zeilen: 458: l.col: 1-6; 459: l.col: 2ff: 460: l.col: 23ff
I. Introduction

Spreading depression (SD), is a physiological/pathophysiological phenomenon which manifests as a propagating wave of neuronal hyperexcitability followed by a transient wake of depression, first identified in the cerebral cortex of rabbits (Leao [sic], 1944; Gorji, 2001). The SD phenomenon is exclusive to the central nervous system and appears to influence both the neuronal and the glial cells. SD can be initiated by different stimuli and so can be directly studied in various in vivo and in vitro experimental models. It was first induced by applying a brief tetanus of faradic stimulation to the rabbit cortex (Leao [sic], 1944; Bures, Buresova & Kriva´nek [sic], 1974; Fig. 1). However, such stimuli could lead to convulsive activity spreading from the stimulated area and so subsequent authors preferred to employ direct current (DC) stimuli (Leao [sic] & Morrison, 1945; Ochs, 1962). 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; Zachar & Zacharova´, 1963). More recent studies have achieved more reliable and reproducible induction of SD by rapidly inserting and retracting hypodermic steel needles (Kaube and Goadsby, 1994; Lambert et al., 1999; Ebersberger et al., 2001). However, one of the most common models of SD initiation is KCl application to the neuronal tissues (Wernsmann et al., 2006; Dehbandi et al., 2008). This model has been proven to be the most reliable stimulus leading to reproducible events on earlier occasions in both nonimaging and imaging studies (Martins-Ferreira et al., 2000; 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 & Sykova, 1998).

Other methods of SD induction are including: (1) metabolic inhibitors such as NaCN and NaN that poison oxidative metabolism and NaF and iodoacetate that primarily interfere with glycolysis; (2) the Na+-K+ ATP-ase inhibitor ouabain has also been used in cortical brain slices; (3) applications of the excitatory amino acids glutamate and aspartate may elicit SD ; (4) local cooling may initiate SD by depressing energy metabolism below a critical level but has proven an irreproducible experimental method. Furthermore, cooling itself raises the threshold for electrically or mechanically induced SD.; (5) there are isolated reports of high-frequency electrical stimulation combined with the administration of pharmacological agents producing SD (Smith et al., 2006).

I. INTRODUCTION

Cortical spreading depression (CSD) refers to a pathophysiological phenomenon which manifests as a propagating wave of neuronal hyperexcitability followed by a transient wake of quiescence first identified in the cerebral cortex of rabbits (Fig. 1) (Leão, 1944; Somjen, 2005).

[page 459]

The CSD phenomenon is exclusive to the central nervous system (CNS) and appears to involve both the neuronal and the glial cell populations. It can be initiated by a range of stimuli and so can be directly studied in different in vivo and in vitro experimental systems. CSD was first induced by applying a brief tetanus of faradic stimulation to the rabbit cortex (Leão, 1944; Bureš, Buresová & Krivánek, 1974). However, such stimuli could lead to convulsive activity spreading from the stimulated area and so subsequent authors preferred to employ direct current (d.c.) stimuli (Leão & Morrison, 1945; Ochs, 1962). [...]

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), but this leaves permanent anatomical changes at the site of application (Syková et al., 2000). [...]

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 & Syková, 1998).

[page 460]

Other CSD triggers have also been used including: (1) metabolic inhibitors such as NaCN and NaN that poison oxidative metabolism and NaF and iodoacetate that primarily interfere with glycolysis (Bureš et al., 1974); (2) the Na+-K+ ATPase inhibitor ouabain has also been used in cortical brain slices (Aquino-Cias, Harmony & Guma, 1967; Menna, Tong & Chesler, 2000); (3) applications of the excitatory amino acids glutamate and aspartate may elicit CSD (Van Harrevald, 1959) but less reliably than KCl (Curatolo et al., 1967); application of 100–250 μmol l-1 glutamate through a microdialysis probe failed to elicit CSD (Obrenovitch & Zilkha, 1995); (4) local cooling may initiate CSD by depressing energy metabolism below a critical level but has proven an irreproducible experimental method (Zachar & Zacharová, 1963). Furthermore, cooling itself raises the threshold for electrically or mechanically induced CSD. Finally (5) there are isolated reports of high-frequency electrical stimulation combined with the administration of pharmacological agents producing CSD (Marshall, 1959; Bureš et al., 1974).

Anmerkungen

The source is mentioned at the very end as one of many sources mentioned on this page. There is no indication that two long paragraphs are taken from it.

Sichter
(Hindemith) Schumann

[8.] Clg/Fragment 018 19 - Diskussion
Bearbeitet: 11. May 2014, 19:27 Schumann
Erstellt: 11. May 2014, 19:08 (Graf Isolan)
Berger et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 18, Zeilen: 19-23
Quelle: Berger et al 2008
Seite(n): 560, Zeilen: right col. 22-32
A conditioning tetanic stimulation was delivered to the white substance of neocortical slices followed by pulses with stimulation parameters identical to control values. The evoked fEPSP was stable for at least 30 min before application of tetanic stimulation (less than 10% variation; Fig. 5). Administration of tetanic stimulation produced a rapid and stable enhancement of the amplitude of the fEPSP in all tested preparations (n = 6, 153 ± 10 % control; Fig. 6). A conditioning tetanic stimulation was delivered to the white substance of neocortical slices after induction of CSD or injection of ACSF followed by pulses with stimulation parameters identical to control values. Evoked field potentials were stable for at least 30 min before application of tetanic stimulation (< 10% variation). Tetanic stimulation in slices treated by ACSF injection (control group) produced a rapid, stable and long-lasting enhancement of the amplitude of fEPSP in all tested preparations (n = 6, 130 ± 2.7% control).
Anmerkungen

Not marked as a citation.

Sichter
(Graf Isolan) Agrippina1

[9.] Clg/Fragment 015 01 - Diskussion
Bearbeitet: 11. May 2014, 19:23 Schumann
Erstellt: 10. May 2014, 00:03 (Graf Isolan)
BauernOpfer, Clg, Fragment, Garrett et al 1994, Gesichtet, SMWFragment, Schutzlevel sysop

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Quelle: Garrett et al 1994
Seite(n): 389, Zeilen: left col. 6-9, 12-26
The boundaries of the neocortical areas can be determined by the distribution pattern of neurons expressing somatostatin mRNA in rat neocortex. The occipital region was stratified, with intensely labelled cells for somatostatin in layers II/III and VI and faintly labelled cells in layer V. The parietal region carried a similar stratification, but more space between intensely labelled cells in layers III and V and between layers V and VI gave the region a three-tiered appearance. The temporal lobe displayed intensely labelled cells dispersed throughout layers III and VI and many in layer V as well as those faintly labelled without any differences among the laminae. The distribution of the cells hybridized for somatostatin mRNA formed two configurations within the frontal region. It was difficult to identify any lamination in the first area, whereas the second area demonstrated stratification reminiscent of the parietal region (Garrett et al., 1994). Our investigation demonstrated that the boundaries of the neocortical areas can be determined by the distribution pattern of neurons expressing somatostatin mRNA. [...] The occipital region was stratified, with insensely labeled cells in layers II/III and VI and faintly labeled cells in layer V. The parietal region carried a similar stratification, but more space between intensely labeled cells in layers III and V and between layers V and VI gave the region a three-tiered appearance. The temporal region displayed intensely labeled cells dispersed throughout layers III and VI and many in layer V as well as those faintly labeled without any breaks between the laminae. The distribution of the cells hybridized for somatostatin mRNA formed two configurations within the frontal region. It was difficult to identify any lamination in the first area, whereas the second area demonstrated a stratification reminiscent of the parietal region, but with only two tiers.
Anmerkungen

Though the source is once given (at the end) nothing is marked as a citation.

Sichter
(Graf Isolan) Schumann

[10.] Clg/Fragment 016 20 - Diskussion
Bearbeitet: 11. May 2014, 19:09 Schumann
Erstellt: 11. May 2014, 18:42 (Graf Isolan)
Berger et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Quelle: Berger et al 2008
Seite(n): 560, Zeilen: left col. 23-31, 45-50
Cortical SD-like events were evaluated with respect to their amplitude, duration and velocity rates. SD duration was defined as the interval between the time of half-maximal voltage shift during onset and recovery of the negative DC potential deflection.

3. Long-term potentiation

Single pulses of electrical stimulation were applied through a bipolar platinum electrode attached to the white matter perpendicular to the recording electrodes. Evoked field excitatory postsynaptic potentials (fEPSP) were recorded in the third layer of neocortical slices. The fEPSP was elicited by adjusting the intensity of stimulation to 50% of that at which population spikes after fEPSP began [to appear.]

Single pulses of electrical stimulation were

applied through a bipolar platinum electrode attached to the white matter perpendicular to the recording electrodes. Evoked field excitatory postsynaptic potentials (fEPSP) were recorded in the third layer of neocortical slices. The fEPSP was elicited by adjusting the intensity of stimulation to ~50% of that at which population spikes after fEPSP began to appear. [...] Spreading depression (SD)-like events were evaluated with respect to their repetition, amplitude, duration and velocity rates. SD duration was defined as the interval between the time of half-maximal voltage shift during onset and recovery of the negative d.c. potential deflection.

Anmerkungen

Not marked as a citation.

Sichter
(Graf Isolan) Agrippina1

[11.] Clg/Fragment 017 01 - Diskussion
Bearbeitet: 11. May 2014, 19:06 Schumann
Erstellt: 11. May 2014, 16:16 (Graf Isolan)
Berger et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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The amplitude of fEPSP 1 ms after the onset was measured for data analysis. In long-term potentiation (LTP) experiments, the cortex was sequentially stimulated once every minute. Ten trains of four pulses (pulse duration 0.1 msec; interpulse interval 50 msec; intensity 5 V) were repeated at intervals of 10 msec. LTP was operationally defined as the mean change in fEPSP amplitude in response to five stimuli given 30 min after tetanic stimulation compared with the mean response to five test pulses applied immediately before the stimulation. Thus % potentiation = [(posttetanus amplitude of fEPSP/baseline amplitude of fEPSP) 1] 100. Tetanic stimulation was applied 60 min after application of drug. The amplitude of fEPSP 1 ms after the onset was measured for data analysis. In long-term potentiation (LTP) experiments, the cortex was sequentially stimulated once every minute. Ten trains of four pulses (pulse duration 0.1 ms; interpulse interval 50 ms; intensity 5 V) were repeated at intervals of 10 s. LTP was operationally defined as the mean change in fEPSP amplitude in response to five stimuli given 30 min after tetanic stimulation compared with the mean response to five test pulses applied immediately before the stimulation. Thus, percentage potentiation = post-tetanus amplitude of fEPSP/baseline amplitude of fEPSP. Tetanic stimulation was applied 30 min after induction of CSD.
Anmerkungen

The source is not given.

Sichter
(Graf Isolan) Agrippina1

[12.] Clg/Fragment 024 19 - Diskussion
Bearbeitet: 11. May 2014, 16:12 Schumann
Erstellt: 10. May 2014, 23:43 (Hindemith)
BauernOpfer, Cervia et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop

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Quelle: Cervia et al 2008
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The primary cause of neuronal death in retinal diseases is ischaemia, a condition that can be considered a final common pathway for injury in different retinal pathologies (Quigley et al., 1995; Levin and Louhab 1996). The peptide somatostatin plays important physiological roles, mostly inhibitory, which have formed the basis for the clinical use of SRIF compounds (Weckbecker et al., 2003; Cervia and Bagnoli 2007), and it may protect the retina against ischaemia in a variety of retinal diseases (Cervia et al., 2008).

[...]

Cervia D, Martini D, Ristori C, Catalani E, Timperio AM, Bagnoli P, Casini G (2008) Modulation of the neuronal response to ischaemia by somatostatin analogues in wild-type and knock-out mouse retinas. J Neurochem 106(5):2224-35.

The primary cause of neuronal death in retinal diseases is ischaemia, a condition that can be considered a final common pathway for injury in different retinal pathologies (Quigley et al. 1985, 1995; Levin and Louhab 1996; Osborne et al. 1999, 2004; Barber 2003). [...] The peptide somatostatin (somatotropin release-inhibiting factor, SRIF) plays important physiological roles, mostly inhibitory, which have formed the basis for the clinical use of SRIF compounds (Weckbecker et al. 2003; Cervia and Bagnoli 2007), and it may protect the retina against ischaemia in a variety of retinal diseases (Cervia et al. 2008).

[...]

Cervia D., Casini G. and Bagnoli P. (2008) Physiology and pathology of somatostatin in the mammalian retina: a current view. Mol. Cell. Endocrinol. 286, 112–122.

Anmerkungen

The source is given in the end for the statement "and it may protect the retina against ischaemia in a variety of retinal diseases". It is not clear to the reader that more is taken from the source including references to the literature.

Note that the reference "Cervia et al. 2008" given in the source refers to a different paper than the reference in the dissertation that has been given at the same place.

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[13.] Clg/Fragment 024 08 - Diskussion
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Intravenous somatostatin (25 μg/min for 20 min) was compared with treatment with ergotamine (250 μg intramuscularly), or placebo in a double-blind trial comprising 72 attacks in eight patients (Sicuteri et al., 1984). Infusion of somatostatin reduced the maximal pain intensity and the duration of pain to a level comparable with intramuscular ergotamine. In a randomized, double-blind study subcutaneous somatostatin was compared with ergotamine (Geppetti et al., 1985). Five patients were treated for three attacks by each of the drugs. Subcutaneous somatostatin and ergotamine were equally beneficial as regards effects on maximal pain intensity and the pain area, but somatostatin was less effective in reduction of the duration of headache.

Sicuteri F, Geppetti P, Marabini S, Lembeck F (1984) Pain relief by somatostatin in attacks of cluster headache. Pain 18(4):359-65.

Intravenous somatostatin 25 μg/min for 20 minutes was compared with ergotamine 250μg intramuscularly or placebo in a double-blind trial comprising 72 attacks in eight patients. [102] Infusion of somatostatin reduced the maximal pain intensity and the duration of pain significantly compared with placebo, and to a degree comparable to intramuscular ergotamine.

In another randomised, double-blind study, subcutaneous somatostatin was compared with ergotamine. [102] Five patients were treated for three attacks by each of the drugs. Subcutaneous somatostatin and ergotamine were equally beneficial as regards effects on maximal pain intensity and the pain area, but somatostatin was less effective in reducing the duration of pain.


[102] Sicuteri F. Geppetti P, Marabini S, et al. Pain relief by somatostatin in attacks of cluster headache. Pain 1984; 18: 359-65

[103] Geppetti P, Brocchi A, Caleri D, et al. Somatostatin for cluster beadache attack. In: Pfaffenrath V, Lundberg PO, Sjaastad O, editors. Updating in headache. Berlin: Spring-Verlag, 1985: 302-5

Anmerkungen

The source named "Geppetti et al., 1985" is missing in the chapter "VI. References".

Different spelling: "randomized" instead of "randomised" – a hint that the text also could have been taken from another source.

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(Hood) Schumann

[14.] Clg/Fragment 012 01 - Diskussion
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[There is a suggestion that the high potassium concentration] in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard and Astrup, 1986). Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex (Hossmann, 1996). A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia (Koroleva et al., 1998). Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological or metabolic damage. 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).

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non- NMDA receptor antagonist and by hypothermia (Mies et al., 1993; Mies et al., 1994).


Hossmann KA (1996) Periinfarct depolarizations. Cerebrovasc Brain Metab Rev 8(3):195-208.

Koroleva VI, Vinogradova LV, Korolev OS (1998) The persistent negative potential provoked in different structures of the rat brain by a single wave of spreading cortical depression. Zh Vyssh Nerv Deiat Im I P Pavlova. 48(4):654-63.

Mies G, Iijima T, Hossmann KA (1993) Correlation between peri-infarct DC shifts and ischaemic neuronal damage in rat. Neuroreport 4(6):709-11.

Mies G, Kohno K, Hossmann KA (1994) Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat. J Cereb Blood Flow Metab. 14(5):802-7.

Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the border zone around old small human brain infarcts. Stroke 17(6):1129-37.

Obeidat AS, Andrew RD (1998) Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation. Eur J Neurosci 10(11):3451-61.

Somjen GG, Aitken PG, Balestrino M, Herreras O, Kawasaki K (1990) Spreading depression-like depolarization and selective vulnerability of neurons. A brief review. Stroke 21(11 Suppl):III179- 83.

There is a suggestion that the high potassium concentration in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia [301,395]. Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex [179]. A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia [218]. Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional

[page 44]

release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological [404] or metabolic [148,170] damage. 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 [180,404]. 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 [311].

SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia [218,219]. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non-NMDA receptor antagonist and by hypothermia [281,282,359].


[148] N.A. Gorelova, J. Krivanek, J. Bures, Functional and metabolic correlates of long series of cortical spreading depression waves in rats, Brain Res. 404 (1987) 379-381.

[170] A.J. Hansen, M. Nedergaard, Brain ion homeostasis in cerebral ischemia, Neurochem. Pathol. 9 (1988) 195-209.

[179] K.A. Hossmann, Periinfarct depolarizations, Cerebrovasc. Brain Metab. Rev. 8 (1996) 195-208.

[180] K.A. Hossmann, Mechanisms of ischemic injury: is glutamate involved?, in: J. Krieglstein, H. Oberpichler-Schwenk (Eds.), Pharmacology of Cerebral Ischemia, Medpharm Scientific, Stuttgart, 1994, pp. 239-251.

[218] VI. Koroleva, J. Bures, TPe use of spreading depression waves for acute and long-term monitoring of the penumbra zone of focal ischemic damage in rats, Proc. Natl. Acad. Sci. USA 93 (1996) 3710-3714.

[219] VI. Koroleva, O.S. Korolev, E. Loseva, J. Bures, TPe effect of MK-801 and of brain-derived polypeptides on the development of ischemic lesion induced by photothrombotic occlusion of the distal middle cerebral artery in rats, Brain Res. 786 (1998) 104-114.

[281] G. Mies, K. Kohno, K.A. Hossmann, MK-801, a glutamate antagonist, lowers flow threshold for inhibition of protein synthesis after middle cerebral artery occlusion of rat, Neurosci. Lett. 155 (1993) 65-68.

[282] G. Mies, K. Kohno, K.A. Hossmann, Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat, J. Cereb. Blood Flow Metab. 14 (1994) 802-807.

[301] M. Nedergaard, J. Astrup, Infarct rim: effect of hyperglycemia on direct current potential and [14C]2-deoxyglucose phosphorylation, J. Cereb. Blood Flow Metab. 6 (1986) 607-615.

[311] A.S. Obeidat, R.D. Andrew, Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation, Eur. J. Neurosci. 10 (1998) 3451-3461.

[359] K. Revett, E. Ruppin, S. Goodall, J.A. Reggia, Spreading depression in focal ischemia: a computational study, J. Cereb. Blood Flow Metab. 18 (1998) 998-1007.

[395] B.K. Siesjo, F. Bengtsson, Calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a unifying hypothesis, J. Cereb. Blood Flow Metab. 9 (1989) 127-140.

[404] G.G. Somjen, P.G. Aitken, M. Balestrino, O. Herreras, K. Kawasaki, Spreading depression-like depolarization and selective vulnerability of neurons. A brief review, Stroke 21 (11 S) (1990) III-179-183.

Anmerkungen

The source is not mentioned here.

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(Hindemith) Schumann

[15.] Clg/Fragment 011 19 - Diskussion
Bearbeitet: 11. May 2014, 00:49 Schumann
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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.

Anmerkungen

Nothing is marked as a citation.

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(Graf Isolan) Schumann

[16.] Clg/Fragment 011 01 - Diskussion
Bearbeitet: 11. May 2014, 00:48 Schumann
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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).
Anmerkungen

Nothing is marked as a citation.

Can also be found in Quelle:Clg/Gorji 2001.

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(Graf Isolan) Schumann

[17.] Clg/Fragment 010 01 - Diskussion
Bearbeitet: 11. May 2014, 00:46 Schumann
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b) SD and epilepsy

SD and epilepsy: regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in migraine. The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red. Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. The small but significant reduction in both of those observed in cerebral hemisphere homolateral to the hypoperfused and hypometabolic areas (Bernardi et al., 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Olesen, 1986).

[page 26]

2.13. SD, epilepsy and migraine:

[...]

rCBF changes in epilepsy have some similarities to those changes in migraine. The human brain frequently has been observed during convulsive seizure. An initial pallor preceding and during the early phase of epileptic attack was reported while the latter part of the fit and post-convulsive state were accompanied by widespread vasodilatation of cerebral vessels. The dilated vessels were first cyanotic, and then for several hours bright red (Dalessio 1980). Positron emission tomography shows a significant reduction of rCBF and oxygen consumption in interictal period and an increased local blood flow in the ictal state in epileptic focus. The small but significant reduction in both of those observed in cereberal hemisphere homolateral to the hypoperfused and hypometabolic areas

[page 27]

(Bernardi et al. 1983, Bonte et al. 1983). Ictal scans revealed a focal or multifocal increase in rCBF and oxygen consumption in an active seizure focus (Frank et al. 1986, Olesen 1986).

Anmerkungen

Nothing is marked as a citation.

Taken from an at that time four years old article of Clg's Dr-advisor. Can also be found in Quelle:Clg/Gorji 2001.

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[18.] Clg/Fragment 009 02 - Diskussion
Bearbeitet: 11. May 2014, 00:44 Schumann
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A few years before, Lashley (1941) explained the visual aura associated with his own ophthalmic migraine attacks as bright scintillations moving across his visual field leaving a blind area in his visual field. Mapping the trajectory of this scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 3 mm/min (Lashley, 1941; Milner, 1958). This report accordingly suggested a possible physiological mechanism for migraine aura in the visual cortex. Thus, one may suggest that the scintillations represent the excitatory phase, while the pursuing blind spot is the inhibitory process of a SD event. Similar conclusions were suggested from blood flow studies (Lauritzen, 1984) that demonstrated that the oligaemia associated with the spread of SD from the occipital cortex showed a very similar propagation velocity to that of the SD itself. A few years before, Lashley (1941) described the visual aura associated with his own ophthalmic migraine syndrome as bright scintillations moving across his visual field leaving a blind area in its wake. Mapping the trajectory of this migrainous scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 3 mm min-1 (Lashley, 1941; Milner, 1958). This report accordingly suggested a possible physiological mechanism for migraine aura in the visual cortex. Thus, one may suggest that the scintillations represent the excitatory phase, while the pursuing blind spot is the inhibitory process of a CSD event. Similar conclusions were suggested from blood flow studies (Lauritzen, 1984) that demonstrated that the oligaemia associated with the spread of CSD from the occipital cortex showed a very similar propagation velocity to that of the CSD itself.
Anmerkungen

The source is not given.

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[19.] Clg/Fragment 008 04 - Diskussion
Bearbeitet: 10. May 2014, 23:40 Schumann
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In the isolated chick retina, human neocortical tissue and cat brain, NMDA receptor antagonists block SD completely. By contrast, in rat hippocampus, glutamate and Ca2+ facilitate SD initiation, whereas NMDA antagonists and low Ca2+]o delay its onset but fail to block SD completely. Given the widespread potential signaling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation.

Both volume-activated ion channels and glial cells probably play important roles in the restoration of normal cellular homeostasis. The former are stimulated during cell swelling, and the latter provide spatial buffering that prevents increased levels of [K+]o and [Glu]o during normal neuronal activity. However, they might also prolong SD: volume-activated ion channels release glutamate during SD; and although gliotoxins prolong SD, they also reduce glutamate efflux from glial cells. SD appears more difficult to evoke in brains of larger animals in which the ratio of glia to neurones tends to be higher, suggesting that glial cells are important for limiting SD activity. Such limiting forces might be greater in the more complexly folded human brain, and could explain the paucity of literature accounts of SD during neurosurgery.

In the isolated chick retinad, human neocortical tissuee and cat brainf, NMDA receptor antagonists block SD completely. By contrast, in rat hippocampus, glutamate (and Ca2+) facilitates SD initiation, whereas NMDA antagonists (and low [Ca2+]o) delay its onset but fail to block SD completelyg–i.

Both volume-activated ion channelsj,k and glial cells probably play important roles in the restoration of normal cellular homeostasis. The former are stimulated during cell swelling, and the latter provide spatial buffering that prevents increased levels of [K+]o and [Glu]o during normal neuronal activity. However, they might also prolong CSD: volume-activated ion channels release glutamate during CSD (Ref. l); and although gliotoxins prolong CSD (Ref. m), they also reduce glutamate efflux from glial cellsn. CSD and PID appear more difficult to evoke in brains of larger animals in which the ratio of glia to neurones tends to be higher, suggesting that glial cells are important for limiting CSD activityo. Such limiting forces might be greater in the more complexly folded human brain, and could explain the paucity of literature accounts of CSD during neurosurgery.

Anmerkungen

Bereft of all its original literary references; nothing is marked as a citation. Is complemented by Clg/Fragment_008_01.

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(Graf Isolan) Singulus

[20.] Clg/Fragment 014 02 - Diskussion
Bearbeitet: 10. May 2014, 23:28 Hindemith
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Somatostatin is produced by neuroendocrine neurons of the periventricular nucleus of the hypothalamus. These neurons project to the median eminence, where somatostatin is released from neurosecretory nerve endings into the hypothalamo-hypophysial portal circulation. These blood vessels carry somatostatin to the anterior pituitary gland, where somatostatin inhibits the secretion of growth hormone from somatotrope cells. The somatostatin neurons in the periventricular nucleus mediate negative feedback effects of growth hormone on its own release; the somatostatin neurons respond to high circulating levels of growth hormone by increasing the release of somatostatin. It is also produced by several other populations that project to other regions of the brain. In particular, there are populations of somatostatin neurons in the arcuate nucleus, the hippocampus and the brainstem nucleus of the solitary tract. Somatostatin is produced by neuroendocrine neurons of the periventricular nucleus of the hypothalamus. These neurons project to the median eminence, where somatostatin is released from neurosecretory nerve endings into the hypothalamo-hypophysial portal circulation. These blood vessels carry somatostatin to the anterior pituitary gland, where somatostatin inhibits the secretion of growth hormone from somatotrope cells. The somatostatin neurons in the periventricular nucleus mediate negative feedback effects of growth hormone on its own release; the somatostatin neurons respond to high circulating concentrations of growth hormone and somatomedins by increasing the release of somatostatin, so reducing the rate of secretion of growth hormone.

Somatostatin is also produced by several other populations that project centrally - i.e. to other areas of the brain, and somatostatin receptors are expressed at many different sites in the brain. In particular, there are populations of somatostatin neurons in the arcuate nucleus, the hippocampus and the brainstem nucleus of the solitary tract.

Anmerkungen

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[21.] Clg/Fragment 013 12 - Diskussion
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The mechanisms whereby somatostatin receptors transduce agonist-induced messages into intracellular responses under different conditions and in different cells are complex. [...] The biological effects of somatostatin are mediated through this family of five G-protein coupled receptors [!] with a high degree of sequence similarity and [!] which have been cloned in the early 1990s. They are encoded by five separate genes, located on five different chromosomes, intronless except for sst2, which is alternatively spliced to generate two isoforms named sst2A and sst2B observed mainly in rat and mouse. They all bind natural peptides, somatostatin 14, somatostatin 28 and cortistatin with similar high affinity (nM range). Only sst5 displays a 10-fold higher affinity for somatostatin 28 (Patel, 1999). Because of naturally occurring somatostatins have short half-lives in circulation (1-3 min), synthetic derivatives have been designed to produce more stable compounds. Among the many hundreds of somatostatin analogs that have been synthesized, two analogs are in common clinical use for the treatment of patients with acromegaly and gastroenteropancreatic (GEP) endocrine tumors: octreotide and lanreotide. A third, vapreotide (Sanvar®) which has been well characterized in preclinical studies for its negative effect on cell proliferation is under clinical trials (Gonzalez-Barcena et al., 2003). The mechanisms whereby somatostatin receptors transduce agonist-induced messages into intracellular responses under different conditions and in different cells are complex. The

biological effects of somatostatin are mediated through a family of five G-protein coupled receptors (GPCR) (sst1-sst5) with a high degree of sequence similarity (39-57 %) and [!] which have been cloned in the early 1990s. They are encoded by 5 separate genes, located on 5 different chromosomes, intronless except for sst2, which is alternatively spliced to generate two isoforms named sst2A and sst2B observed mainly in rat and mouse. They all bind natural peptides, somatostatin 14, somatostatin 28 and cortistatin with similar high affinity (nM range). Only sst5 displays a 10-fold higher affinity for somatostatin 28 (Patel 1999) (Guillermet-Guibert et al., 2005; Weckbecker et al., 2003). Because of naturally occurring

[page 3]

somatostatins have short half-lives in circulation (1-3 min), synthetic derivatives have been designed to produce more stable compounds. Among the many hundreds of somatostatin analogs that have been synthesized, two analogs are in common clinical use for the treatment of patients with acromegaly and gastroenteropancreatic (GEP) endocrine tumors: octreotide and lanreotide. A third, vapreotide (Sanvar®) which has been well characterized in preclinical studies for its negative effect on cell proliferation is under clinical trials (Gonzalez-Barcena et al., 2003).

Anmerkungen

The source is not given.

There are similarities in the preceding sentence (line 8-11, not given in the text above), too. Also the omitted sentence (beginning in line 13) exhibits some similarities.

The unnecessary additional space character before "with a high degree of sequence" indicates the practice of copy & paste. The confusing grammar in this sentence is already given in the corresponding source text, too.

Sichter
(Hindemith), Hood

[22.] Clg/Fragment 013 02 - Diskussion
Bearbeitet: 10. May 2014, 22:36 Hindemith
Erstellt: 10. May 2014, 20:25 (Hindemith)
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Quelle: Pyronnet et al 2008
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Since its discovery three decades ago, somatostatin has attracted much attention because of its functional role in the regulation of a wide variety of physiological functions in the brain, pituitary, pancreas, kidney, gastrointestinal tract, thyroid, adrenals, and immune system. Since its discovery three decades ago as an inhibitor of GH release from the pituitary gland, somatostatin has attracted much attention because of its functional role in the regulation of a wide variety of physiological functions in the brain, pituitary, pancreas, gastrointestinal tract, adrenals, thyroid, kidney and immune system.
Anmerkungen

The source is not given.

Sichter
(Hindemith), Hood

[23.] Clg/Fragment 024 24 - Diskussion
Bearbeitet: 10. May 2014, 22:34 Hindemith
Erstellt: 6. May 2014, 23:36 (Graf Isolan)
BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Stumm et al 2004

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In non-neuronal cells, somatostatin has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by somatostatin receptors. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that somatostatin may influence neurodegeneration after brain ischemia. Activation and upregulation of somatostatin receptors type 2 in perifocal pyramidal neurons after focal ischemia were reported. Upregulation of these receptors is most likely the result of both somatostatin-derived and heterologous signals and may counteract somatostatin desensitization. Excessive activation of somatostatin receptors type 2 [in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in somatostatin receptors type 2 -deficient mice (Stumm et al., 2004).] [Page 11404]

Introduction

[...] In non-neuronal cells, SSTR2 has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by SSTRs. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion (MCAO) affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that SSTRs may influence neurodegeneration after brain ischemia.

[Page 11413]

Conclusion

Together, this study provides the first evidence for activation and upregulation of SSTR2 in perifocal pyramidal neurons after focal ischemia. Upregulation of SSTR2 is most likely the result of both SSTR2-derived and heterologous signals and may counteract SSTR2 desensitization. Excessive activation of SSTR2 in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in SSTR2-deficient mice.

Anmerkungen

The source is mentioned in the end as one of several sources mentioned in this passage. This does not make clear that the whole passage is taken from the source and that some quotations are literal.

Sichter
(Graf Isolan), Hindemith

[24.] Clg/Fragment 007 01 - Diskussion
Bearbeitet: 10. May 2014, 18:50 Singulus
Erstellt: 9. May 2014, 11:54 (Graf Isolan)
Clg, Fragment, Gesichtet, James et al 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 7, Zeilen: 1ff (complete page)
Quelle: James et al 2001
Seite(n): 267, 268, Zeilen: 267:box1, left col. 1-20; 268:left col. 4ff
SD probably starts with a cellular efflux of K+, leading to depolarization and a period of relative electrical silence. The subsequent energy-dependent restitution of ion gradients eventually restores normal neuronal activities. The ionic activity, however, results in a wave of neuronal depolarization propagating away from the elicitation site at a velocity of 3 mm/min. Because the depolarization-restoration process takes 1.5 min, the wave is only ~5 mm deep (James et al., 2001).

SD involves a temporary localized redistribution of different ions between intracellular and extracellular spaces. This ion redistribution is energy dependent. During eliciting of SD the concentration of extracellular K+ [K+]o, rapidly rises (up to 60mM), causing brief neuronal excitation then depolarization and a period of electrical silence during which DC potential at the brain surface falls. In tandem, [Na+]o and [Cl]o levels decrease as these ions enter cells. Consequently, water enters cells, the extracellular space is reduced, and cells swell. Ca2+ ions also move inwards, but slightly later than the outward movement of K+, suggesting that Ca2+ movements follow K+ fluxes. Additional negative ion species move outwards to maintain electrical balance, the excitatory neurotransmitter glutamate probably being the most important (Somjen et al., 2001).

[Page 267]

Cortical spreading depression (CSD) involves a temporary, but major, localized redistribution of ions between intracellular and extracellular compartments. This ion redistribution is energy dependenta, becoming clinically significant in ischaemia when brain metabolism is impaired. During CSD initiation the concentration of extracellular K+, [K+]o, rapidly rises, causing brief neuronal excitation then depolarization and a period of electrical silence during which the direct current (DC) potential at the brain surface falls. In tandem, [Na+]o and [Cl]o levels decrease as these ions enter cells. Consequently, water enters cells, the extracellular space is reduced, and cells swellb. Ca2+ ions also move inwards, but slightly later than the outward movement of K+, suggesting that Ca2+ movements follow K+ fluxes. Additional negative ion species move outwards to maintain electrical balance, the excitatory neurotransmitter glutamate probably being the most importantc.

[Page 268]

CSD probably starts with a cellular efflux of K+, leading to depolarization and a period of relative electrical silence (Box 1). The subsequent energy-dependent restitution of ion gradients eventually restores normal neuronal activity. The ionic activity, however, results in a wave of neuronal depolarization propagating away from the initiation site at a velocity of ~3 mm.min−1. Because the depolarization-restoration process takes ~1.5 min, the wave is only ~5 mm deep.

Anmerkungen

Although the source is given (once inbetween) nothing has been marked as a citation.

Sichter
(Graf Isolan) Singulus

[25.] Clg/Fragment 009 11 - Diskussion
Bearbeitet: 10. May 2014, 18:42 Singulus
Erstellt: 8. May 2014, 18:58 (Graf Isolan)
BauernOpfer, Clg, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop

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Seite: 9, Zeilen: 11-34
Quelle: Gorji 2001
Seite(n): 35, 36, Zeilen: 35:right col. 35-44; 36:left col. 42-56 - right col. 1-14
Magnetoencephalographic studies in human revealed that the magnetic signals were seen in migraine patients but not in patients suffering from other forms of headache or normal controls. Three distinctive signal patterns; suppression of spontaneous cortical activity, slow field changes and large-amplitude waves, were observed strictly in migraine patients. In some patients with migraine, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals (Welch et al, 1993). A recent study strongly supports the link between SD and the aura period in human visual cortex. High-field functional magnetic resonance imaging (MRI) was used to detect blood oxygenation level-dependent (BOLD) changes during visual aura in three migraineurs. A focal increase in BOLD signals developed first in extrastriate cortex and spread at the velocity of 3.5 ± 1.1 mm/min over occipital cortex. These initial BOLD features were consistent with scintillations and paralleled by decreases in the stimulus-driven MR oscillations. Increasing in BOLD signals was followed by a decrease in the mean MR signal. This phase appeared to correspond to the localized scotoma and MR stimulus-induced response remained suppressed. Within 15±3 min, both BOLD signals and MR stimulus-induced response recovered. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as CSD did not cross prominent sulci (Hadjikhani et al., 2001). The most common symptoms during the aura phase in migraine are visual. As mentioned, spreading oligemia and excitation wave of aura symptoms start in occipital lobe and propagate anteriorly. Altering the ionic makeup of the extracellular fluid reversibly raises or lowers the susceptibility to SD. Glial cells act as spatial buffer explicitly for potassium by taking potassium up and carrying it from regions of high concentration to neighbouring regions of low concentration. In human the lowest glial-neuronal ratio is in the primary visual cortex (Fig. 2; Gorji, 2001).

Gorji A (2001); Spreading depression: a review of the clinical relevance. Brain Res Brain Res Rev. 38(1-2):33-60.

Hadjikhani N, Sanchez Del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RB, Sorensen AG, Moskowitz MA (2001) Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci U S A 10; 98 (8): 4687-92.

Welch KM, Barkley GL, Tepley N, Ramadan NM (1993) Central neurogenic mechanisms of migraine. Neurology 43(6 Suppl 3):S21-5.

[Page 35]

Magnetoencephalographic studies in human revealed that the magnetic signals were seen in migraine patients but not in patients suffering from other forms of headache or normal controls. Three distinctive signal patterns; suppression of spontaneous cortical activity, slow field changes and large-amplitude waves, were observed strictly in migraine patients. In some migraineurs, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals [455].

[Page 36]

A recent study strongly supports the link between SD and the aura period in human visual cortex. High-field functional MRI was used to detect blood oxygenation level-dependent (BOLD) changes during visual aura in enhanced in three migraineurs. A focal increase in BOLD signals developed first in extrastriate cortex and spread at the velocity of 3.5±1.1 mm/min over occipital cortex. These initial BOLD features were consistent with scintillations and paralleled by decreases in the stimulus-driven MR oscillations. Increasing in BOLD signals was followed by a decrease in the mean MR signal. This phase appeared to correspond to the localized scotoma and MR stimulus-induced response remained suppressed. Within 15±3 min, both BOLD signals and MR stimulus-induced response recovered. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD who suffer from migraine with aura, they found that the signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as CSD did not cross prominent sulci [162].

The most common symptoms during the aura phase in migraine are visual. As mentioned, spreading oligemia and excitation wave of aura symptoms start in occipital lobe and propagate anteriorly. Altering the ionic makeup of the extracellular fluid reversibly raises or lowers the susceptibility to SD. Glial cells act as spatial buffer explicitly for potassium by taking potassium up and carrying it from regions of high concentration to neighboring regions of low concentration [324]. In human the lowest glial-neuronal ratio is in the primary visual cortex [20].


[20] P. Baily, G. von Bonin, in: The Isocortex of Man, University of Illinois Press, Urbana, IL, 1951.

[162] N. Hadjikhani, M. Sanchez Del Rio, O. Wu, D. Schwartz, D. Bakker, B. Fischl, K.K. Kwong, F.M. Cutrer, B.R. Rosen, R.B. Tootell, A.G. Sorensen, M.A. Moskowitz, Mechanisms of migraine aura revealed by functional MRI in human visual cortex, Proc. Natl. Acad. Sci. USA 98 (2001) 4687–4692.

[324] R.K. Orkand, J.G. Nicholls, S.W. Kuffler, Effect of nerve impulses on the membrane potential of glial cells in the central nervous system of amphibia, J. Neurophysiol. 29 (1966) 788–806.

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

Anmerkungen

Nothing has been marked as a citation.

Sichter
(Graf Isolan) Singulus

[26.] Clg/Fragment 008 01 - Diskussion
Bearbeitet: 10. May 2014, 18:18 Singulus
Erstellt: 10. May 2014, 17:50 (Graf Isolan)
Clg, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Seite: 8, Zeilen: 1-4, 7-9
Quelle: Gorji 2001
Seite(n): 34, Zeilen: left col. 44-46 - right col. 1-7
No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the spread of SD probably involves the release and diffusion of the chemical mediators, most likely K+ and glutamate into the interstitial fluid. [...] Given the widespread potential signaling capacities of Ca2+ waves, observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation. No explanation of the propagation of SD has been suggested that accounts for all the facts presently proven. The hypothesis that gained wide acceptance is that the spread of SD probably involves the release and diffusion of the chemical mediators, most likely K+ and glutamate into the interstitial fluid [440]. Given the widespread potential signaling capacities of Ca2+ waves [332], observations of the interactions between astrocytes and neurons in cell culture have suggested that Ca2+ waves play a role in SD initiation and propagation [231,299].

[231] PE. Kunkler, R.P. Kraig, Calcium waves precede electrophysiological changes of spreading depression in hippocampal organ cultures, J. Neurosci. 18 (1998) 3416-3425.

[299] M. Nedergaard, Direct signaling from astrocytes to neurons in cultures of mammalian brain cells, Science 263 (1994) 1768-1771.

[332] V. Parpura, T.A. Basarsky, F. Liu, K. Jeftinija, S. Jeftinia, P.G. Haydon, Glutamate-mediated astrocyte-neuron signaling, Nature 369 (1994) 744-747.

[440] A. Van Harreveld, Two mechanisms for spreading depression in the chicken retina, J. Neurobiol. 9 (1978) 419-431.

Anmerkungen

Nothing is marked as a citation. Complements Clg/Fragment_008_04.

Sichter
(Graf Isolan) Singulus

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