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24 gesichtete, geschützte Fragmente: Plagiat

[1.] Tmm/Fragment 039 23 - Diskussion
Bearbeitet: 28. April 2014, 21:16 Hindemith
Erstellt: 23. April 2014, 21:40 (Hindemith)
BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006

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Seventy per cent of CSD waves propagating from temporal cortex slices penetrated to adjacent entorhinal cortex slices and stopped there, whereas the remaining 30% reached CA1 and CA3 regions of the hippocampal slices (Wernsmann et al., 2006). On the other hand, CSD elicited from the somatosensory neocortex of anaesthetized rats did not penetrate into the hippocampus (Wernsmann et al., 2006). This suggests that the CSD recording in slices offers better conditions for SD propagation probably due to weakening of intrahippocampal inhibitory mechanisms. Seventy per cent of CSD waves propagating from temporal cortex slices penetrated to adjacent entorhinal cortex slices and stopped there, whereas the remaining 30% reached CA1 and CA3 regions of the hippocampal slices. On the other hand, CSD elicited from the somatosensory neocortex of anaesthetized rats did not penetrate into the hippocampus. This suggests that the CSD recording in slices offers better conditions for SD propagation probably due to weakening of intrahippocampal inhibitory mechanisms.
Anmerkungen

The source is mentioned twice, but the copied text continues after the second reference and includes a conclusion the reader will attribute to the author of the thesis, not to Wernsmann et al (2006). Furthermore, nothing is marked as a quotation although the text has been taken literally.

Sichter
(Hindemith) Agrippina1

[2.] Tmm/Fragment 040 03 - Diskussion
Bearbeitet: 28. April 2014, 18:29 Schumann
Erstellt: 23. April 2014, 21:26 (Hindemith)
BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006

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Seite: 40, Zeilen: 3-20, 23-28
Quelle: Wernsmann et al 2006
Seite(n): 1108, 1109, Zeilen: 1108: r.col: last 5 lines; 1109: l.col: 1-22
The entorhinal cortex, a palaeocortical area, receives projections from secondary and higher associative areas of the neocortex. Regions of both ipsilateral frontal and temporal lobes are found to contribute afferents to this region of the brain. The association areas from the primary sensory modalities of vision, audition, and somesthesis project to multimodal convergence areas in the frontal and parietal lobes (Pandya & Kuypers, 1969). Both multimodal regions project in turn to the cingulate gyrus on the medial surface of the hemisphere, which contributes a heavy supply of afferents to the presubiculum and entorhinal cortex (Jones & Powell, 1970). Therefore, the entorhinal cortex is a final cortical link between the sensory systems of the neocortex and the hippocampus of the limbic system and plays a role as a filter between these two structures. From the entorhinal inputs, the hippocampus receives highly complex and differentiated signals, coding information about the properties of the applied stimuli. The entorhinal cortical neurons constitute the direct perforant path and the crossed temporoammonic path to the hippocampus. They terminate on dendritic branches of CA1–CA3 and the dentate fascia neurons (Van Hoesen et al., 1972). Transient sensory cortical dysfunction induced by abortive SD enhanced hippocampal activity (Wernsmann et al., 2006). This suggests an inhibitory tone mediated through neocortical influence on hippocampal plasticity. In our study, application of GABAA blocker inhibited propagation of SD to the hippocampus via the entorhinal cortex. This may related to the manipulation of this inhibitory inputs of the entorhinal cortex to the hippocampus. Our conclusion is supported by recent evidence indicating that elimination of cortical input resulted in increased reactivity and complete disappearance of habituation, with prolongation of tonic responses in the hippocampus (Vinogradova, 2001). Lesions of the entorhinal cortex in adolescent rats also resulted in enhancement of spontaneous locomotor activities, an effect possibly mediated by postsynaptic hypersensitivity (Sumiyoshi et al., 2004). The entorhinal cortex, a palaeocortical area, receives projections from secondary and higher associative areas of the neocortex. Regions of both ipsilateral frontal and temporal lobes are found to contribute afferents to this region of the brain. The association areas from the primary sensory modalities of vision, audition and somesthesis project

[page 1109]

to multimodal convergence areas in the frontal and parietal lobes (Pandya & Kuypers, 1969). Both multimodal regions project in turn to the cingulate gyrus on the medial surface of the hemisphere, which contributes a heavy supply of afferents to the presubiculum and entorhinal cortex (Jones & Powell, 1970). Thus, the entorhinal cortex is a final cortical link between the sensory systems of the neocortex and the hippocampus of the limbic system. From the entorhinal input, the hippocampus receives highly complex and differentiated signals, coding information about the properties of the applied stimuli. The entorhinal cortical neurons constitute the direct perforant path and the crossed temporoammonic path to the hippocampus. They terminate on dendritic branches of CA1–CA3 and the dentate fascia neurons (Van Hoesen et al., 1972). In the present study, transient sensory cortical dysfunction induced by abortive SD enhanced hippocampal activity. This suggests an inhibitory tone mediated through neocortical influence on hippocampal plasticity. Our conclusion is supported by recent evidence indicating that elimination of cortical input resulted in increased reactivity and complete disappearance of habituation, with prolongation of tonic responses in the hippocampus (Vinogradova, 2001). Lesions of the entorhinal cortex in adolescent rats also resulted in augmented spontaneous locomotor activity, an effect possibly mediated by postsynaptic hypersensitivity (Sumiyoshi et al., 2004).

Anmerkungen

The source is mentioned once somewhere in the middle of the paragraph just like many other references to the literature. Nothing is marked as a quotation. The reader would never guess that the whole passage is taken from the source more or less literally.

Only one sentence is not taken from the source and has not been counted. Note that even the expression "Our conclusion is supported by recent evidence[...]" is taken from the source (which, by the way, was five years old at the time of writing of the thesis).

Sichter
(Hindemith) Agrippina1

[3.] Tmm/Fragment 038 18 - Diskussion
Bearbeitet: 28. April 2014, 17:54 Hindemith
Erstellt: 23. April 2014, 21:50 (Hindemith)
BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006

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Seite(n): 1108, Zeilen: r.col:16-28
Intrinsic optical imaging as well as bioelectrical recordings revealed different patterns of SD propagation in hippocampal and entorhinal slices (Buchheim et al., 2002; Wernsmann et al., 2006). All data indicated of a resistance of the entorhinal cortex for penetration by cortical SD. Although the exact mechanisms responsible for difficulty of cortical SD propagation to the entorhinal cortex are not clear, some hypotheses can be derived from experimental data. A traditional view assumes that the entorhinal cortex faithfully transmits neocortical inputs to the hippocampus and the hippocampus inputs to the neocortex (Naber et al., 1999). More recent evidence suggests that the entorhinal cortex is more than a simple relay between the neocortex and hippocampus. The entorhinal cortices contribute to the gating of impulses between these brain structures. Local inhibition and intrinsic membrane properties of entorhinal neurons are major factors limiting impulse traffic across the entorhinal cortex (Pelletier et al., 2004). Intrinsic optical imaging also revealed different patterns of SD propagation in hippocampal and entorhinal slices (Buchheim et al., 2002). Although the exact mechanisms responsible for different propagation patterns of SD are not clear, some hypotheses can be derived from experimental data. A traditional view assumes that the entorhinal cortices faithfully transmit neocortical inputs to the hippocampus and vice versa (Naber et al., 1999). More recent evidence suggests that the entorhinal cortices are more than a simple relay between the neocortex and hippocampus. Entorhinal cortices contribute to the gating of impulses between these structures. Local inhibition and intrinsic membrane properties of entorhinal neurons are major factors limiting impulse traffic across the entorhinal cortex (Pelletier et al., 2004).
Anmerkungen

The source is given, but not as reference for the entire passage, but as one of two references for the statement "Intrinsic optical imaging as well as bioelectrical recordings revealed different patterns of SD propagation in hippocampal and entorhinal slices"

Sichter
(Hindemith) Agrippina1

[4.] Tmm/Fragment 039 01 - Diskussion
Bearbeitet: 28. April 2014, 17:01 Hindemith
Erstellt: 23. April 2014, 21:35 (Hindemith)
Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Verschleierung, Wernsmann et al 2006

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In line with this, physiological studies have disclosed the existence of powerful inhibition in the entorhinal cortex (Finch et al., 1986; Jones & Buhl, 1993; Funahashi & Stewart, 1998), which may act to abort the propagation of SD.

In addition, some studies indicated relative difficulties of SD occurrence in the hippocampus compared with the entorhinal cortex (Dalby & Mody, 2003; Faria & Mody, 2004). The failure of cortical SD to spread to the hippocampus was reported earlier (Fifkova, 1964). The release of glutamate is essential to the propagation of cortical SD (Van Harreveld & Fifkova, 1973). Several studies have shown that glutamate acts via NMDA receptors during the generation and propagation of SD (Mody et al., 1987; Gorji, 2001). The NMDA receptors are assembled from NR1 subunits and at least one subtype of the four members of the NR2(A–D) subunits family. NR2B subunits are essential to the generation and propagation of SD in the entorhinal cortical slices (Faria & Mody, 2004). The physiological characteristics and possibly the localization of NR2B subunits at synapses differ between the entorhinal cortex and the hippocampus (Gordey et al., 2001; Faria & Mody, 2004), which, in turn, may influence SD penetration into the hippocampus.

Consistent with this, physiological studies have disclosed the existence of powerful inhibition in the entorhinal cortex (Finch et al., 1986; Jones & Buhl, 1993; Funahashi & Stewart, 1998), which may act to abort the propagation of SD.

Furthermore, some studies indicated a relative resistance of SD occurrence in the hippocampus compared with entorhinal cortex (Dalby & Mody, 2003; Faria & Mody, 2004). The failure of cortical SD to propagate to the hippocampus was reported earlier (Fifkova, 1964). The release of glutamate is essential to the propagation of cortical SD (Van Harreveld & Fifkova, 1973). Several studies have shown that glutamate acts via NMDA receptors during the generation and propagation of SD (Mody et al., 1987; Gorji, 2001). The NMDA receptor is a heterotetramer assembled from NR1 subunits and at least one subtype of the four members of the NR2(A–D) subunits family. NR2B subunits are essential to the generation and propagation of SD in entorhinal cortical slices (Faria & Mody, 2004). The physiological characteristics and possibly the localization of NR2B subunits at synapses differ between the entorhinal cortex and the hippocampus (Gordey et al., 2001; Faria & Mody, 2004), which, in turn, may influence SD penetration into the hippocampus.

Anmerkungen

The source is not mentioned here. It will be mentioned in passing in the next paragraph.

Sichter
(Hindemith) Agrippina1

[5.] Tmm/Fragment 041 01 - Diskussion
Bearbeitet: 28. April 2014, 17:01 Hindemith
Erstellt: 23. April 2014, 21:18 (Hindemith)
BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006

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Seite(n): 1109, Zeilen: l.col: 23-39, 50-62, r.col: 1-4
LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting modifications of which individual synapses are capable. LTP remains one of the prime candidates for mediating learning and memory as well as many other forms of experience-dependent plasticity (Malenka & Bear, 2004). Functional disruption of neocortical input to the hippocampus induced by abortive SD in both in vitro and ex vivo experiments enhanced the LTP in the CA1 hippocampal area ipsilateral to SD initiation (Wernsmann et al., 2006). Enhancement of LTP by abortive SD was NMDA receptor dependent. Our data indicate the modulatory role of the changes of synaptic strength by LTP induction on SD propagation. In line with our results, CSD visualized using manganese-enhanced MRI following topical application of KCl to the exposed rat cortex revealed signal enhancement in CA1–3 areas, the subiculum and the dentate gyrus of the hippocampus (Henning et al., 2005).

Some evidence implicates the hippocampus in spatial memory and navigation, learning and emotion (Jensen & Lisman, 2005). This structure is also related primarily to the control of gross movements, such as locomotion and changes in posture, and involved in certain aspects of the pituitary–adrenocortical system. Amnesia, emotional disturbances, hyperactivity, yawning, and fluid retention were observed in hippocampal dysfunction as well as during migraine attacks (Bures et al., 1974; Isaacson & Pribram, 1975; Dalessio, 1980; Daquin et al., 2001). SD in animal experiments also elicits similar symptoms (Gorji, 2001). SD-like changes occur with visual aura in patients with migraine (Hadjikhani et al., 2001). Propagation of depolarizing waves in sensory systems of the neocortex may directly affect primary sensory modalities and induce aura symptoms such as visual hallucinations. SD, both indirectly via the effect on entorhinal input to the hippocampus or directly by propagation to the hippocampal structure, may disturb the hippocampal function and lead to symptoms such as amnesia or hyperactivity during migraine attacks.

LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting modifications of which individual synapses are capable. LTP remains one of the prime candidates for mediating learning and memory as well as many other forms of experience-dependent plasticity (Malenka & Bear, 2004). In the present study, functional disruption of neocortical input to the hippocampus induced by abortive SD in both in vitro and ex vivo experiments enhanced the LTP in the CA1 hippocampal area ipsilateral to SD initiation. Enhancement of LTP by abortive SD was NMDA receptor dependent, as APV blocked LTP induction. Further propagation of SD to the hippocampus, conversely, inhibits LTP. These data indicate the modulatory role of SD on the efficacy of the hippocampal synaptic transmission. In line with our results, CSD visualized using manganese-enhanced MRI following topical application of KCl to the exposed rat cortex revealed signal enhancement in CA1–3 areas, the subiculum and the dentate gyrus of the hippocampus (Henning et al., 2005).

[...] Some evidence implicates the hippocampus in spatial memory and navigation, learning and emotion (Jensen & Lisman, 2005). This structure is also related primarily to the control of gross movements, such as locomotion and changes in posture, and involved in certain aspects of the pituitary–adrenocortical system. Amnesia, emotional disturbances, hyperactivity, yawning and fluid retention were observed in hippocampal dysfunction as well as during migraine attacks (Bures et al., 1974; Isaacson & Pribram, 1975; Dalessio, 1980; Daquin et al., 2001). SD in animal experiments also elicits similar symptoms (Gorji, 2001). SD-like changes occur with visual aura in patients with migraine (Hadjikhani et al., 2001). Propagation of depolarizing waves in sensory systems of the neocortex may directly affect primary sensory modalities and induce aura symptoms such as visual hallucinations. SD, either indirectly via the effect on entorhinal input to the hippocampus or directly by propagation to the hippocampal structure, may disturb the hippocampal function and lead to symptoms such as amnesia or hyperactivity during migraine attacks.

Anmerkungen

The source is mentioned once somewhere in the middle of the paragraph just like many other references to the literature. Nothing is marked as a quotation. The reader would never guess that the whole passage is taken from the source more or less literally.

Sichter
(Hindemith) Agrippina1

[6.] Tmm/Fragment 013 01 - Diskussion
Bearbeitet: 28. April 2014, 16:45 Schumann
Erstellt: 23. April 2014, 20:41 (Hindemith)
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[As memories in humans depend initially on the medial temporal lobe system, including the] hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966). Furthermore, propagation of SD in the hippocampus was believed to play a role in migraine pain by triggering nociceptive activation of the caudal trigeminal nucleus (Kunkler and Kraig, 2003). Classical studies investigated hippocampal SD more often by implantation of KCl into the hippocampus and induction of SD directly in the tissue. Little information is available on the effects of cortical SD on hippocampal activity. Because altered neural circuit function can be seen remote from the SD propagation site, using in vitro brain models, the effects of different substances as well as electrical stimulation on propagation of SD between the neocortex and the hippocampus was investigated. As memories in humans depend initially on the medial temporal lobe system, including the hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966; Kapp & Schneider, 1971). Furthermore, propagation of SD in the hippocampus was believed to play a role in migraine pain by triggering nociceptive activation of the caudal trigeminal nucleus (Kunkler & Kraig, 2003). Classical studies investigated hippocampal SD more often by implantation of KCl into the hippocampus and induction of SD directly in the tissue. Little information is available on the effects of cortical spreading depression (CSD) on hippocampal activity. Because altered neural circuit function can be seen remote from the SD propagation site (Bures et al., 1961; Albe-Fessard et al., 1984; Moskowitz et al., 1993; Kunkler & Kraig, 2003; Gorji et al., 2004), using in vitro and ex vivo / in vitro brain models, the effects of neocortical SD on the synaptic plasticity of hippocampal tissues were tested.
Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Agrippina1

[7.] Tmm/Fragment 012 22 - Diskussion
Bearbeitet: 28. April 2014, 16:45 Schumann
Erstellt: 23. April 2014, 20:32 (Hindemith)
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The hippocampus has direct and important functional interactions with brain areas likely to be important to migraine, such as the areas associated with vision, emotions and neuroendocrine homeostasis. The connection between entorhinal cortex and hippocampus is regarded as an important loop responsible for the processing of sensory information (Vaisanen et al., 1999). Thus, these medial temporal lobe structures may play a crucial role in the development of somatosensory and neuropsychotic symptoms in neurological disorders such as epilepsy and migraine (Eid et al. 1995). As memories in humans depend initially on the medial temporal lobe system, including the [hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966).] The hippocampus has direct and important functional interactions with brain areas likely to be important to migraine, such as the areas associated with vision, emotions and neuroendocrine homeostasis. The connection between entorhinal cortex and hippocampus is regarded as an important loop responsible for the processing of sensory information (Vaisanen et al., 1999). Thus, these medial temporal lobe structures may play a crucial role in the development of somatosensory and neuropsychotic symptoms in neurological disorders such as epilepsy and migraine (Eid et al., 1995). As memories in humans depend initially on the medial temporal lobe system, including the hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966; Kapp & Schneider, 1971).
Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Agrippina1

[8.] Tmm/Fragment 015 01 - Diskussion
Bearbeitet: 28. April 2014, 15:49 Schumann
Erstellt: 23. April 2014, 20:12 (Hindemith)
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Seite(n): 16, 17, Zeilen: 16: 20ff - 17: 1ff
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.

Long-term potentiation

Single pulses of electrical stimulation were applied through a bipolar platinum electrode attached to the white matter perpendicular to the recording electrode in the entorhinal cortex. Evoked field excitatory postsynaptic potentials (fEPSP) were recorded in the third layer of the entorhinal cortex. The fEPSP was elicited by adjusting the intensity of stimulation to ~50% of that at which population spikes after fEPSP began to appear. The amplitude of fEPSP 1 ms after the onset was measured for data analysis. In longterm 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.

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

[page 17]

to appear. 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.

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[9.] Tmm/Fragment 010 01 - Diskussion
Bearbeitet: 28. April 2014, 15:49 Schumann
Erstellt: 23. April 2014, 19:20 (Hindemith)
Fragment, Gesichtet, Granz 2009, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Tmm

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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. A small but significant reduction in both of those was 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).

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 depolarisations 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).

Propagation of SD

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. 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.

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. 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.

[page 10]

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 12]

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).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann

[10.] Tmm/Fragment 009 01 - Diskussion
Bearbeitet: 28. April 2014, 15:49 Schumann
Erstellt: 23. April 2014, 16:39 (Hindemith)
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[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 of SD in oxygen/glucose-deprived (ischemic) tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic areas increase in opacity (Obeidat and Andrew, 1998).

C) SD and epilepsy: 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, blocking of K+ channels, e.g., by 4-aminopyridine, activation of NMDA receptors, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of T-type Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for initiation of both epileptiform burst discharges and SD in experimental animal models (Gorji, 2001). By all abovementioned 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, 1982). Penetration of cortical SD 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, 1982). SD was observed in association with epilepsy in patients suffering from brain vascular disorders (Fabricius et al., 2008). Regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in [migraine.]

b) SD and epilepsy

SD and epilepsy: regional cerebral blood flow (rCBF) changes in epilepsy have some similarities to those changes in migraine.

[page 11]

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 was observed in association with epilepsy in patients suffering from brain vascular disorders (Fabricius et al., 2008).

[page 12]

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).

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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. There is a suggestion that the high potassium concentration in the ischemic focus initiates diffusion of K+ into the adjacent normally superfused cortex and triggers SD-like deflections propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard et al., 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 strong enough to support sufficiently intensive diffusion of active substances into the intact neocortex (Hossmann, 1996). A SD wave elicited 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 120 minutes 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 events are significantly longer than those occurring in normoxic neocortex 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. 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. There is a suggestion that the high potassium concentration

[page 12]

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.

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Figure 2. A schematic pattern of propagation of spreading depression in human brain. Traces recorded from human tissues. Vertical propagation of spreading depression reveals a very slow velocity of DC-negative deflection recorded in human brain tissues obtained during epilepsy surgery.

B) SD and cerebrovascular diseases: SD was observed in patients suffering from brain ischemia/infarction, brain haemorrhage, and subarachnoid haemorrhage. The damage to cerebral tissue depends on a complex series of physiological responses and degenerative 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’.]

07 source Tmm.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.

[page 11]

c) SD and cerebrovascular diseases

SD and cerebrovascular diseases: SD was observed in patients suffering from brain ischemia/infarction, brain haemorrhage, and subarachnoid haemorrhage. 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’.

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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). In line with these data, 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). 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 propagates anteriorly. Altering the ionic makeup of the extracellular fluid reversibly raises or lowers the susceptibility to SD. Glial cells act as spatial buffer especially for potassium by taking potassium up and carrying it from regions of high concentration to neighbouring areas of low concentration. Regarding anatomical studies in human, the lowest glial–neuronal ratio is in the primary visual cortex (Fig. 2; Gorji, 2001). 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). [...] 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).
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[Direct modulation of electrical activity of cortical neurons by the locally] spreading wave can lead to neurological symptoms (e.g. the aura phase of migraine). These same neuronal processes can also alter the neurochemistry of cortical and subcortical structures, modulating oxygen distribution and cell survival in these structures and change the behaviour. These problem has not been addressed before, mainly because SD induces such a short depression in each cortical loci, that transient neurochemical changes cannot be examined with conventional approaches, for example by microdialysis.

A) SD and migraine with aura: A few years before discovery of SD, Lashley (1941) explained his visual aura associated with his own ophthalmic migraine attacks as bright scintillations moving across the visual field leaving a blind area in his visual field. Mapping the trajectory of his scotoma across his visual field gave a predicted velocity over a retinotopically organised visual cortex of approximately 2-3 mm/min (Lashley, 1941; Milner, 1958). This report accordingly suggested a possible physiological mechanism for migraine aura in the visual cortex. Thus, it may be suggested that the scintillations represent the excitatory phase, while the pursuing blind spot is the inhibitory process of a SD wave. 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 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 closed to SD propagation velocity (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 about fifteen minutes, both BOLD signals and MR stimulus-induced [response recovered.]

Direct modulation of electrical activity of cortical neurons by the locally spreading wave can lead to neurological symptoms (e.g. the aura phase of migraine). These same neuronal processes can also alter the neurochemistry of subcortical structures, modulating oxygen distribution, cell survival in these structures and behavior. This problem has not been addressed before, mainly because SD induces such a short depression in each cortical loci, that transient neurochemical changes cannot be examined with conventional approaches, for example by microdialysis.

[page 9]

a) SD and migraine with aura

SD and migraine with aura: 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 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.

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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) application of the Na+-K+ ATP-ase inhibitor ouabain; (2) applications of the excitatory amino acids glutamate and aspartate; (3) administration of metabolic inhibitors such as NaCN and NaN that poison oxidative metabolism and NaF and iodoacetate that primarily interfere with glycolysis; (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).

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.

SD and neurological disorders

Processes similar to SD phenomenon in animal cortex are thought to occur in different neurological disorders in humans. These conditions are migraine with aura, brain trauma, ischemia/infarction, brain haemorrhage, epilepsy, and transient global amnesia (Gorji, 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).

[page 8]

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.

1. Clinical relevance of SD

Processes similar to SD in animal cortex are thought to take place in a number of neuropathological conditions in humans. These conditions include migraine with aura, brain trauma, ischemia/ infarction, epilepsy, hemorrhage and transient global amnesia (see Gorji, 2001 for a recent review on clinical aspects of SD).

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Figure 1.: Aristides Azevedo Pacheco Leão. Journal of Nourophysiology, 1944 (classic figure of SD discovery), Alterations of electrical activities recorded from a rabbit during propagation of spreading depression (SD). Traces reveal propagation of flattening of epileptiform burst potentials elicited by spreading of cortical SD as well as gradual propagating recovery of these activities.

SD can be initiated by different stimuli and so can be directly studied in various in vivo and in vitro experimental animal models. It was first induced by applying a brief tetanus of faradic stimulation to the rabbit neocortex (Leao, 1944; Bures et al., 1974; Fig. 1). However, such stimuli could lead to convulsive activity spreading from the stimulated area and so other investigators employed direct current (DC) stimuli (Leao & 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, 1944; Zachar and 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 non-imaging and imaging studies (Martins-Ferreira [et al., 2000; Bradley et al., 2001).]

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, 1944; Bures, Buresova & Kriva´nek, 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 & 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, 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 non-imaging and imaging studies (Martins-Ferreira et al., 2000; Bradley et al., 2001).

[page 7]

03 source Tmm.png

Fig. 1: Aristides Azevedo Pacheco Leão. Journal of Nourophysiology, 1944, Changes of bioelectrical activities recorded from a rabbit during propagation of spreading depression (SD). Traces reveal propagation of flattening epileptiform field potentials induced by spreading of cortical SD as well as spreading recovery of these activities.

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Given the widespread potential signalling 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. Given the widespread potential signaling [sic] 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.
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Statistical analysis

All data are given as mean ± SEM. The data were statistically analysed using the Mann–Whitney Rank Sum test. Significance was established when the probability values were less than 0.05. The investigations were approved by the local ethics committee (Tierversuchsgenehmigung, Bezirksregierung Münster, Deutschland, AZ: 50.0835.1.0, G79/2002).

6. Statistical analysis

All data are given as mean ± SEM. The data were statistically analysed using the Mann–Whitney Rank Sum test. [...] Significance was established when the probability values were less than 0.05. The investigations were approved by the local ethics committee (Tierversuchsgenehmigung, Bezirksregierung Münster, Deutschland, AZ: 50.0835.1.0, G79/2002).

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While the content is hardly original, the words have been copied literally.

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Electrophysiological recordings

Extracellular field potentials were recorded with glass microelectrodes (150 mmol/l NaCl; 2–10 MΩ) connected to the amplifier by an Ag/AgCl–KCl bridge in the third layer of temporal neocortical tissues as well as in the entorhinal cortex and hippocampal CA1 and CA3 areas. Field potentials were traced by an ink-writer and recorded by a digital oscilloscope.

Induction of neocortical SD

SD was elicited by KCl microinjection. 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 sixth layer of the neocortical slices. A high-pressure pulse was applied to inject an amount of K+ in the tissue sufficient to induce cortical SD (tip diameter: 2 m; [sic] injection pressure 0.5–1.0 bar applied for 200-300 ms, two injections, 1–3 nl per pulse).

1. Electrophysiological recordings

Extracellular field potentials were recorded with glass microelectrodes (150 mmol/l NaCl; 2–10 MΩ) connected to the amplifier by an Ag/AgCl–KCl bridge in the third and the fifth layers of neocortical tissues. Field potentials were traced by an ink-writer and recorded by a digital oscilloscope.

2. Induction of neocortical SD

SD was elicited by KCl microinjection. 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 sixth layer of the neocortical slices. A high-pressure pulse was applied to inject an amount of K+ in the tissue sufficient to induce cortical SD (tip diameter: 2 m; [sic] injection pressure 0.5–1.0 bar applied for 200-300 ms, two injections, 1–3 nl per pulse).

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[The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3] μM, 0.5–2 bar; 500–800 ms, 3–5 nl). Drugs were released through microelectrodes on to the surface of the slices. The abovementioned drugs were administered focally through microelectrodes on to slices (electrode tip diameter 2–3 μM, 0.5–2 bar; 500–800 ms, 3–5 nl). Drugs were released through microelectrodes on to the surface of the slices.
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Material and methods

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

Material and methods

Slice preparation

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

Anmerkungen

The source is not mentioned.

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[22.] Tmm/Fragment 012 01 - Diskussion
Bearbeitet: 27. April 2014, 00:35 Hindemith
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Patent gap junctions may provide a path not only for electric current and for ions but also for intracellular “second” messengers and other active ingredients in cytosol. SD has frequently been interpreted as a diffusion-reaction process whose velocity of spread is governed by the rate of the reaction, which could involve the release of some substance from cells that then acted on the cell membrane of adjacent cells. As there are reasons for doubting a decisive role of either K or of glutamate, we are proposing an alternative hypothesis, involving the exchange of chemical signals not through the interstitial space but by way of gap junctions. The autocatalytic reaction so initiated would alter the membrane from the inside, instead of acting on receptors on the outside.

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

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

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

[page 11]

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

Anmerkungen

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[23.] Tmm/Fragment 011 04 - Diskussion
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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 than to the antecedent events. Among antecedents heralding the onset of SD that have been reported, are a slight increase of extracellular potassium, a small positive shift preceding the fast negative shift of the extracellular potential and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Higashida et al., 1974). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Higashida et al., 1974). Not all of these early signs are obligatory prodromals of the large, accelerating, regenerative depolarization that is typical of the process.

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

Widely accepted hypotheses hold that the primary event responsible for both the initiation and the propagation of SD is the release of some substance from neuronal elements to the extracellular compartment, which initially excites and then depresses adjacent neurons. The slowness of diffusion of the mediator would account for the low velocity of SD propagation. Among the substances proposed to mediate SD propagation are potassium (Grafstein, 1963; Bures et al., 1974) and excitatory amino acids (Fabricius et al., 1993). There are, however, observations that are difficult to reconcile with either of these two propositions.

SD had been interpreted as a composite process or a sequence of several linked events. To solve its genesis, a most important question concerns identification of the very first step in the chain reaction. In the extant literature, however, generally more attention has been given to the major depolarization and the attending extracellular potential shift (AI’,)[sic] than to the antecedent events. Among antecedents heralding the onset of SD that have been reported, are

[page 10]

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

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

Anmerkungen

The source is not mentioned.

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

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Introduction

Spreading depression (SD) is a pathophysiological phenomenon which exhibits as a propagating wave of neuronal and glial hyperexcitability of few seconds followed by a transient wave of depression of few minutes and later subsides with another longduration hyperexcitability, first identified in the cerebral cortex of rabbits (Leao, 1944; Somjen, 2001; Gorji, 2001). The SD phenomenon is exclusive to the central nervous system and influences both the neuronal and the glial cells in different parts of the central nervous system including both brain and spinal cord.

SD propagated in all neuronal tissues in both vertical and horizontal directions. 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 2-5 mm/min. Because the depolarization-restoration process takes 1.5 min, the wave is only ~5mm deep (Smith et al., 2006). [...]

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, extracellular sodium ([Na+]o) and chloride ([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 crucial (Nicholson and Sykova, 1998; Somjen et al., 2001).

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, 1944; Gorji, 2001). The SD phenomenon is exclusive to the central nervous system and appears to influence both the neuronal and the glial cells.

[page 7]

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).

Anmerkungen

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Note that sub- and superscripts have been lost in Tmm

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