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Angaben zur Quelle [Bearbeiten]

Autor     Justin M. Smith, Daniel P. Bradley, Michael F. James, Christopher L.-H. Huang
Titel    Physiological studies of cortical spreading depression
Zeitschrift    Biological Reviews
Herausgeber    Cambridge Philosophical Society
Ausgabe    81
Jahr    2006
Seiten    457–481
DOI    10.1017/S1464793106007081
URL    http://onlinelibrary.wiley.com/doi/10.1111/j.1469-185X.2006.tb00214.x/abstract

Literaturverz.   

yes
Fußnoten    yes
Fragmente    2


Fragmente der Quelle:
[1.] Clg/Fragment 006 01 - Diskussion
Zuletzt bearbeitet: 2014-05-11 19:41:27 Schumann
BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Smith et al 2006

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Untersuchte Arbeit:
Seite: 6, Zeilen: 1ff (complete)
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).

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[2.] Clg/Fragment 009 02 - Diskussion
Zuletzt bearbeitet: 2014-05-11 00:44:36 Schumann
Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Smith et al 2006, Verschleierung

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Untersuchte Arbeit:
Seite: 9, Zeilen: 2-11
Quelle: Smith et al 2006
Seite(n): 458, Zeilen: l.col: 6-22
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

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