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19 gesichtete, geschützte Fragmente: Plagiat

[1.] Amh/Fragment 005 01 - Diskussion
Bearbeitet: 6. May 2014, 21:40 Schumann
Erstellt: 30. April 2014, 10:19 (Hindemith)
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Introduction

Spreading depression (SD) is a propagating wave of depolarisation associated by a depression of the neuronal bioelectrical activity for a period of minutes. [...] SD appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression. A crucial manifestation of SD is a propagating negative potential with an amplitude of 10–30 mV and a duration of more than 0.5–1 min, which may be preceded or succeeded by a positive fluctuation of variable amplitude and duration. Underlying this cellular depolarisation is a dramatic change in the distribution of micromilieu ions between extra- and intracellular compartments. Potassium and proton release from the cells, while sodium, calcium and chloride enter together with water causing cells to swell and the volume of the extracellular compartment to be decreased. SD is accompanied by an increase of glucose utilization and O2 consumption. Recovery of SD depends on energy metabolism.

1. Introduction

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


[...]

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(Hindemith) Schumann

[2.] Amh/Fragment 005 16 - Diskussion
Bearbeitet: 6. May 2014, 21:40 Schumann
Erstellt: 24. April 2014, 16:50 (Graf Isolan)
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The first paper on SD, titled "Spreading depression of activity in the cerebral cortex" appeared in 1944, written by a young Brazilian investigator, Aristides Leão, working at the Harvard laboratory. Leão wanted to study the electrocorticogram (ECoG) of experimental epilepsy in anesthetized rabbits, but he was distracted from his original goal by an unexpected flattening of the ongoing normal bioelectrical activity that took the place of the anticipated epileptiform field potentials.The silencing of the ECoG trace crept slowly over the cortex, from one recording electrode pair resting on the cortical surface to the one beside it. According to Leão, SD and propagating focal seizures were related phenomena, generated by the same cellular elements, an inference later supported by others. [page 1066]

The first, seminal paper on SD, titled “Spreading depression of activity in the cerebral cortex” (213) appeared in 1944, written by a young and unknown Brazilian inves-

[page 1067]

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


213. LEÃO AAP. Spreading depression of activity in the cerebral cortex. J Neurophysiol 7: 359–390, 1944.

428. VAN HARREVELD A AND STAMM JS. Spreading cortical convulsions and depressions. J Neurophysiol 16: 352–366, 1953.

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(Graf Isolan) Schumann

[3.] Amh/Fragment 005 25 - Diskussion
Bearbeitet: 6. May 2014, 21:41 Schumann
Erstellt: 30. April 2014, 09:56 (Hindemith)
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This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under different experimental conditions. It has been also observed in human neocortical tissue in vitro and in human hippocampus as well as striatum and neocortex in vivo. SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold. This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under various experimental conditions [47]. It has been also observed in human neocortical tissue in vitro [16,17,149] and in human hippocampus as well as striatum [408] and neocortex [272] in vivo.[...]

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


[...]

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[4.] Amh/Fragment 006 01 - Diskussion
Bearbeitet: 6. May 2014, 21:41 Schumann
Erstellt: 30. April 2014, 10:06 (Hindemith)
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Conversely, the susceptibility of SD initiation is lowered or the occurrence of SD is prevented in previously susceptible tissue by solution with increased Mg2+ or NaCl, or with the Na+ replaced by certain other cations. SD also is triggered by various modes of mechanical, chemical and electrical stimulation. Conversely, the susceptibility of SD initiation is lowered or the occurrence of SD is prevented in previously susceptible tissue by solution with increased Mg2+ or NaCl, or with the Na+ replaced by certain other cations. SD also is triggered by various modes of mechanical, chemical and electrical stimulation [47].

[...]

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The passage starts on the previous page: Amh/Fragment_005_25

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[5.] Amh/Fragment 006 05 - Diskussion
Bearbeitet: 7. May 2014, 17:46 Hindemith
Erstellt: 7. May 2014, 14:47 (Schumann)
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The unparalleled increase in extracellular potassium concentration ([K+]o) is accompanied by a precipitous drop in extracellular chloride concentration ([Cl-]o), extracellular sodium concentration ([Na+]o), and extracellular calcium concentration ([Ca2+]o), suggesting that K+ leaving neurons is exchanged against Na+ and Ca2+ that are entering and increased up to 60 mM. [Ca2+]o decreases from its normal level of 1.2-1.5 mM to <0.3 mM. Cations are not exchanged one for one between intra- and extracellular solutions, for the reduction in [Na+]o is greater than the increase in [K+]o. The concomitant drop in [Cl-]o indicates that some of the Na+ entering the cells is accompanied by Cl. It has been suggested that the deficit in extracellular anions is made up by anions leaving the cytosol. Organic anions, including glutamate, have been shown to be released during SD, although some of the glutamate originates from glial cells. The unparalleled increase in [K+]o (35, 221, 232, 434) is accompanied by a precipitous drop in [Cl-]o, [Na+]o, and [Ca2+]o (78, 124, 128, 187, 281, 283, 373, 448), suggesting that K+ leaving cells is exchanged against Na+ and Ca2+ that are entering (281, 360). [Ca2+]o decreases from its normal level of 1.2-1.5 mM to ,0.3 mM. Cations are not exchanged one for one between intra- and extracellular solutions, for the reduction in [Na+]o is greater than the increase in [K+]o (267). The concomitant drop in [Cl-]o indicates that some of the Na+ entering the cells is accompanied by Cl-. Nicholson (281) suggested that the deficit in extracellular anions is made up by anions leaving the cytosol. Indeed, organic anions, including glutamate, have been shown to be released during SD (71, 81, 395, 397, 420), although some of the glutamate comes from glial cells (170, 171, 394).

[...]

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[6.] Amh/Fragment 007 01 - Diskussion
Bearbeitet: 6. May 2014, 21:07 WiseWoman
Erstellt: 29. April 2014, 15:20 (Graf Isolan)
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[An exact and complete balance sheet of all ingredients displaced during SD is yet to be completed, however, so much larger than that of the interstitial] compartment that neurons need to give up but a fraction of the K+ they contain to achieve a many fold rise in [K+]o. Calculations based on the simultaneously recorded levels of [Na+]o and [K+]o and the known fractional volume of the interstitial space in hippocampal tissue indicate that a much reduced but still substantial trans-membrane potassium concentration gradient remains standing during SD.

The unusual magnitude of the changes in extracellular ion concentrations created the impression that intra- and extracellular ion concentrations equilibrate during SD, and this idea was bolstered by the nearly complete depolarization of neurons during SD. The volume of the cytosol is, however, so much larger than that of the interstitial space that cells need to give up but a fraction of the K+ they contain to achieve a many fold rise in [K+]o. Calculations based on the simultaneously recorded levels of [Na+]o and [K+]o and the known fractional volume of the interstitial space in hippocampus indicate that a much reduced but still substantial transmembrane K+ concentration gradient remains standing during SD.

An exact and complete balance sheet of all ingredients displaced during SD is yet to be completed, however.

The unusual magnitude of the changes in extracellular ion concentrations created the impression that intra- and extracellular ion concentrations equilibrate during SD, and this idea was bolstered by the nearly complete depolarization of neurons during SD (57, 137, 391; see sect. IIH). The volume of the cytosol is, however, so much larger than that of the interstitial space that cells need to give up but a fraction of the K1 they contain to achieve a manyfold rise in [K+]o. Calculations based on the simultaneously recorded levels of [Na+]o and [K+]o and the known fractional volume of the interstitial space in hippocampus indicate that a much reduced but still substantial transmembrane K+ concentration gradient remains standing during HSD (267) (Figs. 4A and 7D).

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Amh uses the same passage of text twice on the same page. The first time around there are still some slight changes to the original text ("potassium" instead of "K+"). The second time the match is exact

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(Graf Isolan) Schumann

[7.] Amh/Fragment 007 14 - Diskussion
Bearbeitet: 7. May 2014, 18:43 Schumann
Erstellt: 7. May 2014, 18:17 (Hindemith)
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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 propagation of SD probably involves the release of different chemical mediators, most likely K+ and glutamate into the interstitial fluid. 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 may also play a role in SD 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. 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 (Gorji 2001).
Anmerkungen

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Note that the almost identical text can be found in the source Gorji (2001): Amh/Dublette/Fragment_007_14

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[8.] Amh/Fragment 008 00 - Diskussion
Bearbeitet: 7. May 2014, 18:47 Schumann
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08a diss Amh.png

Figure 2. Propagation of cortical spreading depression and its electrophysiological recordings.

08a source Amh.png

Fig. 1. Propagation of a negative DC-potential wave after injection of KCl in a neocortical slice. [...]

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[9.] Amh/Fragment 008 02 - Diskussion
Bearbeitet: 6. May 2014, 21:42 Schumann
Erstellt: 30. April 2014, 09:44 (Hindemith)
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SD belongs in the domain of the pathophysiology of the brain, and there are reasons to believe that it is involved in different clinical disorders, including migraine, cerebrovascular diseases, head injury and transient global amnesia. SD belongs in the domain of the pathophysiology of the brain, and there are reasons to believe that it is involved in some clinical disorders, including migraine, cerebrovascular diseases, head injury and transient global amnesia.
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The source is not mentioned. The passage starts on the previous page: Amh/Fragment_007_14.

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[10.] Amh/Fragment 009 04 - Diskussion
Bearbeitet: 6. May 2014, 20:25 Singulus
Erstellt: 29. April 2014, 15:57 (Graf Isolan)
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The designation migraine with aura denotes the syndrome of headache associated with characteristic sensory, motor, or visual symptoms, usually gradually developed over 5–20 min and lasting less than 60 min. The most common symptoms in aura phase are visual arising from dysfunction of occipital lobe neurons. The positive (stimulative) neurological symptoms, e.g., flashing lights are usually followed by negative (suppressive) ones, e.g., scotoma or hemianopia in this phase. 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 migraine patients, magnetic signals were also recorded between attacks. The same magnetic fields appeared during the propagation of SD in the cortex of anesthetized animals. High-field functional 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 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 neocortical SD did not cross prominent sulci. [page 34]

The designation migraine with aura denotes the syndrome of headache associated with characteristic sensory, motor, or visual symptoms, usually gradually developed over 5–20 min and lasting less than 60 min. The most common symptoms in aura phase are visual arising from dysfunction of occipital lobe neurons. The positive (stimulative) neurological symptoms, e.g., flashing lights are usually followed by negative (suppressive) ones, e.g., scotoma or hemianopia in this phase.

[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]

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 signal followed the retinotopic progression of the visual percept. Spreading BOLD signal changes as CSD did not cross prominent sulci [162].


[...]

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Not marked as a citation, the source is not mentioned.

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(Graf Isolan), Hindemith

[11.] Amh/Fragment 009 26 - Diskussion
Bearbeitet: 6. May 2014, 20:27 Hindemith
Erstellt: 24. April 2014, 14:09 (Graf Isolan)
Amh, Eikermann-Haerter and Moskowitz 2008, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Recent investigations provide early insights into mechanisms that lead to trigeminovascular activation. SD is the first endogenous event identified upstream to trigeminovascular activation that appears to be noxious in experimental models. Neocortical SD, originally described by Leão. The slow spread of SD at 3–5 mm/min matches the propagation velocity of wave fronts in the Belousov–Zhabotinsky reaction, that is, a thermodynamic chemical reaction that shows the properties of a nonlinear chemical oscillator even in a Petri dish. Recent studies provide early insights into endogenous mechanisms that lead to trigeminovascular activation. CSD is the first endogenous event identified upstream to trigeminovascular activation that appears to be noxious in experimental models. CSD, originally described by Leão [73], is an intense depolarization of neuronal and glial membranes accompanied by a massive disruption of ionic gradients and loss of membrane resistance [5]. The slow spread of CSD at 3–5 mm/min matches the propagation velocity of wave fronts in the Belousov–Zhabotinsky reaction, that is, a thermodynamic chemical reaction that shows the properties of a nonlinear chemical oscillator even in a Petri dish [74].

3 Eikermann-Haerter K, Moskowitz MA. Pathophsyiology of aura. In: Silberstein BR, editor. Wolff’s headache and other head pain. 2007. pp. 121–132.
This chapter gives a comprehensive overview on pathophysiology of migraine aura and summarizes important findings in both basic and clinical research.

73 Leão AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944; 7:359–390.

74 Biosa G, Bastianoni S, Rustici M. Chemical waves. Chemistry 2006; 12:3430–3437.

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[12.] Amh/Fragment 010 01 - Diskussion
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Unlike an epileptic seizure, which spreads asynchronously to activate adjacent brain, SD begins within a synchronously activated brain space.

In experimental animals, SD stimulates ipsilateral trigeminal axons that surround cortical blood vessels. SD causes a breakdown of the blood–brain barrier by mechanisms dependent on matrix metalloproteinase-9. Furthermore, neocortical SD causes ipsilateral extravasation of plasma proteins in dura mater, serving as an experimental marker of trigeminal nerve activation; it also induces c-Fos expression within the trigeminal nucleus caudalis. These findings and a transcription MRI study suggest that intense cortical perturbations like repeated SD can open the blood–brain barrier, thereby activating the trigeminovascular system. SD releases chemicals such as H+, K+, nitric oxide, and neurotransmitters into the extracellular space. It has been hypothesized that released molecules reach the pial surface by diffusion and accumulate in proximity to trigeminovascular afferents. Extracellular K+ levels about 60 mmol/l were measured in the pial space during SD.

Consistent with an upstream role for SD, prolonged application of migraine prophylactic drugs suppresses SD in rats as a proposed mechanism of action. In line with the growing clinical recognition that prolonged administration of prophylactic drugs is important to achieve maximum therapeutic efficacy, treatment extension beyond 3–4 weeks also maximizes the inhibitory effects of topiramate, valproate, methysergide, amitriptyline, and propranolol on SD.

Unlike an epileptic seizure, which spreads asynchronously to activate adjacent brain, CSD begins within a synchronously activated brain space [75].

In experimental animals, CSD stimulates ipsilateral trigeminal axons that surround cortical blood vessels [7]. CSD causes a breakdown of the blood–brain barrier by mechanisms dependent on matrix metalloproteinase-9 [76]. Furthermore, CSD causes ipsilateral extravasation of plasma proteins in dura mater, serving as an experimental marker of trigeminal nerve activation [6]; it also induces c-Fos expression within the trigeminal nucleus caudalis [8]. These findings and a recent transcription MRI study [77] suggest that intense cortical perturbations like repeated CSD can open the blood–brain barrier, thereby activating the trigeminovascular system. CSD releases chemicals such as H+, K+, nitric oxide, and neurotransmitters into the extracellular space. It has been hypothesized that released molecules reach the pial surface by bulk diffusion and accumulate in proximity to trigeminovascular afferents. Extracellular K+ levels greater than 40 mmol/l were measured in the pial space during CSD.

Consistent with an upstream role for CSD, prolonged administration of migraine prophylactic drugs suppresses CSD in rats as a proposed mechanism of action [24]. In line with the growing clinical recognition that prolonged administration of prophylactic drugs is important to achieve maximum therapeutic efficacy, treatment extension beyond 3–4 weeks also maximizes the inhibitory effects of topiramate, valproate, methysergide, amitriptyline, and DL propranolol on CSD [24].


6 Moskowitz MA. Genes, proteases, cortical spreading depression and migraine: impact on pathophysiology and treatment. Funct Neurol 2007;22:133–136.

This work reviews important developments supporting the view of cortical spreading depression as an upstream driver of both migraine aura and pain.

7 Bolay H, Reuter U, Dunn AK, et al. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med 2002; 8:136–142.

8 Moskowitz MA, Nozaki K, Kraig RP. Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. J Neurosci 1993; 13:1167–1177.

24 Ayata C, Jin H, Kudo C, et al. Suppression of cortical spreading depression in migraine prophylaxis. Ann Neurol 2006; 59:652–661.

75 Kunkler PE, Hulse RE, Schmitt MW, et al. Optical current source density analysis in hippocampal organotypic culture shows that spreading depression occurs with uniquely reversing currents. J Neurosci 2005; 25:3952–3961.

76 Gursoy-Ozdemir Y, Qiu J, Matsuoka N, et al. Cortical spreading depression activates and upregulates MMP-9. J Clin Invest 2004; 113:1447–1455.

77 Liu CH, You Z, Ren J, et al. Noninvasive delivery of gene targeting probes to live brains for transcription MRI. FASEB J 2007 [Epub ahead of print].
This study uses an innovative transcription MRI technique to visualize specific cerebral mRNA in vivo. It validates noninvasive delivery of novel magnetic resonance probes to the brains of live animals after acute neurological disorders.

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[13.] Amh/Fragment 010 22 - Diskussion
Bearbeitet: 7. May 2014, 13:28 Schumann
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Amh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wikipedia Dopamine 2009

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In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors; D1, D2, D3, D4 and D5, and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area Dopamine is also a neurohormone released by the hypothalamus.

Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the ventral tegmental area of the midbrain, the substantia nigra pars compacta, and the arcuate nucleus of the hypothalamus

In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors — D1, D2, D3, D4 and D5, and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.[1] Dopamine is also a neurohormone released by the hypothalamus. [...]

[...]

Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the ventral tegmental area (VTA) of the midbrain, substantia nigra pars compacta, and arcuate nucleus of the hypothalamus.


1. http://www.encyclopedia.com/ doc/1O87-ventraltegmentalarea.html Reference for VTA.

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[14.] Amh/Fragment 011 01 - Diskussion
Bearbeitet: 7. May 2014, 15:50 Schumann
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Quelle: Meador-Woodruff et al 1996
Seite(n): 17, Zeilen: abstract: 1ff
The distributions of the transcripts encoding the five dopamine receptors have been determined in the human striatum and selected regions of the neocortex. In the prefrontal cortex as well as the temporal neocortex D1 and D4 receptor mRNAs are the most abundant, although the other three transcripts are seen at lower levels. In the occipital neocortex, D1 receptor mRNA is the most abundant, D3 the rarest, while the other three transcripts are present at modest levels of expression (Meador-Woodruff et al., 1996). The distributions of the transcripts encoding the five dopamine receptors have been determined in the human striatum and selected regions of the neocortex. [...] In the prefrontal cortex D1 and D4 receptor mRNAs are the most abundant, although the other three transcripts are seen at lower levels. A similar pattern is seen in the temporal neocortex. In the occipital cortex, D1 receptor mRNA is the most abundant, D3 the rarest, while the other three transcripts are present at modest levels of expression.
Anmerkungen

The source is given, but the literal quotations are not marked as such and it is also not clear to the reader that all three sentences are taken from the source.

Sichter
(Hindemith) Schumann

[15.] Amh/Fragment 012 18 - Diskussion
Bearbeitet: 7. May 2014, 13:19 Schumann
Erstellt: 24. April 2014, 19:00 (Graf Isolan)
Amh, Fragment, Gesichtet, KomplettPlagiat, Peroutka 1997, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 12, Zeilen: 18-22
Quelle: Peroutka 1997
Seite(n): 650, Zeilen: 4-7
Most migraine symptoms can be induced by dopaminergic stimulation. Moreover, there is dopamine receptor hypersensitivity in migraineurs, as demonstrated by the induction of yawning, nausea, vomiting, hypotension, and other symptoms of a migraine attack by dopaminergic agonists at doses that do not affect nonmigraineurs. Most migraine symptoms can be induced by dopaminergic stimulation. Moreover, there is dopamine receptor hypersensitivity in migraineurs, as demonstrated by the induction of yawning, nausea, vomiting, hypotension, and other symptoms of a migraine attack by dopaminergic agonists at doses that do not affect nonmigraineurs.
Anmerkungen

Identical, not marked as a citation.

Sichter
(Graf Isolan) Agrippina1

[16.] Amh/Fragment 012 27 - Diskussion
Bearbeitet: 7. May 2014, 13:19 Schumann
Erstellt: 24. April 2014, 19:11 (Graf Isolan)
Amh, BauernOpfer, Fragment, Gesichtet, Peroutka 1997, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 12, Zeilen: 27-29
Quelle: Peroutka 1997
Seite(n): 654, Zeilen: left col. 45 - right col. 1-6
In a large subgroup of migraineurs, dopamine acts as an endogenous protagonist in the pathophysiology of the disorder. Antagonism of this protagonist neurotransmitter therefore results in symptomatic relief of both the headache and associated symptoms (Peroutka, 1997).

Peroutka SJ. (1997) Dopamine and migraine. Neurology. 49:650-6.

These data support the hypothesis that at least in a large subgroup of migraineurs, dopamine acts as an endogenous protagonist in the pathophysiology of the disorder. Antagonism of this protagonist neurotransmitter therefore results in symptomatic relief of both the headache and associated symptoms.
Anmerkungen

Though the source is given nothing has been marked as a citation.

Sichter
(Graf Isolan) Agrippina1

[17.] Amh/Fragment 014 26 - Diskussion
Bearbeitet: 7. May 2014, 18:50 Schumann
Erstellt: 7. May 2014, 18:12 (Hindemith)
Amh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sheikh 2009, Verschleierung

Typus
Verschleierung
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 14, Zeilen: 26-30
Quelle: Sheikh 2009
Seite(n): 14, Zeilen: 1ff
Statistical analysis

All data are given as mean ± SEM. The data were statistically analysed using the Mann-Whitney Rank Sum test. Multiple comparisons were performed by analysis of variance test (ANOVA) for repeated measures followed by a Holm-Sidak’s 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).]

Statistical analysis

All data are given as mean ± SEM. The data were statistically analysed using the Mann-Whitney Rank Sum test. Multiple comparisons were performed by analysis of variance test (ANOVA) for repeated measures followed by a Duncan's test. Significance was established when the probability values were less than 0.05. The investigations were approved by the local ethics committee (Ethikkommission der Ärztekammer Westfalen-Lippe und der Medizinischen Fakultät der Universität Münster; April 18, 2000, Reg.Nr.: OIVSpe).

Anmerkungen

The source is not given although almost the exact same words are used.

Sichter
(Hindemith) Schumann

[18.] Amh/Fragment 023 10 - Diskussion
Bearbeitet: 6. May 2014, 21:43 Schumann
Erstellt: 29. April 2014, 22:33 (Graf Isolan)
Amh, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Stanwood 2008, Verschleierung

Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 23, Zeilen: 10-26
Quelle: Stanwood 2008
Seite(n): 4, 5, Zeilen: 4:1-16; 5:5-10
Dopamine is widely distributed in the central nervous system and serves a variety of functions in the mature brain, including control of movement, cognition, endocrine responses, and reward. Dysfunction of dopaminergic system plays an important role in many neurological and psychiatric disorders, including schizophrenia, Parkinson's disease, attention-deficit

hyperactivity disorder, and drug addiction (Arnsten and Li, 2005; Biederman and Faraone, 2005; Kalivas and Volkow, 2005). Dopamine receptors are G protein-coupled receptors, characterized by an extracellular N-terminal region, intracellular C-terminal region, and seven membrane-spanning regions. There are two subfamilies of DA receptors, D1 receptors and D2 receptors, based on their pharmacological profiles and sequence homology (Lachowicz and Sibley, 1997; Missale et al., 1998). D1 receptors, including the D1 and D5 receptor subtypes, catalyze synthesis of cAMP. D2 receptors, including the D2, D3, and D4 receptor subtypes, inhibit cAMP synthesis. The receptors also affect activation of potassium channels and mitogen-activated protein kinases (Neve et al., 2004; Beaulieu et al., 2005). Several studies have identified binding partners for the D2 receptor including coreceptors, signaling molecules, and scaf-folding proteins (Smith et al., 1999; Macey et al., 2004; Negyessy and Goldman-Rakic, 2005; So et al., 2005; Liu et al., 2006 , 2007; Rashid et al., 2007; Kim et al., 2008).


Arnsten AF, Li BM. (2005) Neurobiology of executive functions: catecholamine influences on prefrontal cortical functions. Biol Psychiatry. 1;57:1377-84.

Beaulieu JM, Sotnikova TD, Marion S, Lefkowitz RJ, Gainetdinov RR, Caron MG.( 2005) An Akt/beta-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. Cell. 29;122:261-73.

Biederman J, Faraone SV. (2005) Attention-deficit hyperactivity disorder. Lancet. 16-22;366:237-48.

Kalivas PW, Volkow N, Seamans J. (2005) Unmanageable motivation in addiction: a pathology in prefrontal-accumbens glutamate transmission.Neuron. 3;45:647-50.

Kim JH, Cho EY, Min C, Park JH, Kim KM. (2008) Characterization of functional roles of DRY motif in the 2nd intracellular loop of dopamine D2 and D3 receptors. Arch Pharm Res. 31:474-81.

Lachowicz JE, Sibley DR. (1997) Molecular characteristics of mammalian dopamine receptors. Pharmacol Toxicol. 81:105-13.

Liu Y, Teeter MM, DuRand CJ, Neve KA. (2006) Identification of a Zn2+-binding site on the dopamine D2 receptor. Biochem Biophys Res Commun. 20;339:873-9.

Macey TA, Gurevich VV, Neve KA. (2004) Preferential Interaction between the dopamine D2 receptor and Arrestin2 in neostriatal neurons. Mol Pharmacol. 66:1635-42.

Missale C, Nash SR, Robinson SW, Jaber M, Caron MG. (1998) Dopamine receptors: from structure to function. Physiol Rev. 78:189-225.

Negyessy L, Goldman-Rakic PS. (2005) Subcellular localization of the dopamine D2 receptor and coexistence with the calcium-binding protein neuronal calcium sensor-1 in the primate prefrontal cortex. J Comp Neurol. 8;488:464-75.

Rashid AJ, So CH, Kong MM, Furtak T, El-Ghundi M, Cheng R, O'Dowd BF, George SR. ( 2007) D1-D2 dopamine receptor heterooligomers with unique pharmacology are coupled to rapid activation of Gq/11 in the striatum. Proc Natl Acad Sci U S A. 9;104:654-9.

Smith FD, Oxford GS, Milgram SL. (1999) Association of the D2 dopamine receptor third cytoplasmic loop with spinophilin, a protein phosphatase-1-interacting protein. J Biol Chem. 9;274:19894-900.

So CH, Varghese G, Curley KJ, Kong MM, Alijaniaram M, Ji X, Nguyen T, O'dowd BF, George SR. (2005) D1 and D2 dopamine receptors form heterooligomers and cointernalize after selective activation of either receptor. Mol Pharmacol. 68:568-78.

[page 4]

Dopamine (DA) is widely distributed in the central nervous system (CNS) and serves a variety of functions in the mature brain, including control of movement, cognition, endocrine responses, and reward. Dopaminergic abnormalities contribute to many neurological and psychiatric disorders, including schizophrenia, Parkinson’s disease, attention-deficit hyperactivity disorder, and drug addiction (Arnsten and Li, 2005; Biederman and Faraone, 2005; Girault and Greengard, 2004; Goldman-Rakic, 1998; Kalivas and Volkow, 2005; Kiyatkin, 1995; Nestler, 2001).

DA receptors are G protein-coupled receptors (GPCRs), characterized by an extracellular N-terminus region, intracellular C-terminus region, and seven membrane spanning regions. There are two subfamilies of DA receptors, D1-like receptors and D2-like receptors, based on their pharmacological profiles and sequence homology (Lachowicz and Sibley, 1997; Missale et al., 1998). D1-like receptors, including the D1 and D5 receptor sub-types, catalyze synthesis of cAMP. D2-like receptors, including the D2, D3, and D4 receptor subtypes, inhibit cAMP synthesis. The receptors also affect activation of potassium channels, mitogen-activated protein kinases, and Akt (Beaulieu et al., 2005; Neve et al., 2004).

[page 5]

Several previous studies have identified binding partners for the D2 receptor including co-receptors, signaling molecules, and scaffolding proteins (see Fig. 1) (Beaulieu et al., 2005; Beaulieu et al., 2007; Binda et al., 2002; Free et al., 2007; Fuxe et al., 2005; Kim et al., 2008; Liu et al., 2006; Liu et al., 2007; Macey et al., 2004; Negyessy and Goldman-Rakic, 2005; Rashid et al., 2007; Smith et al., 1999; So et al., 2005).


Arnsten AF and Li BM (2005) Neurobiology of executive functions: catecholamine influences on prefrontal cortical functions. Biol Psychiatry 57(11):1377-1384.

Beaulieu JM, Sotnikova TD, Marion S, Lefkowitz RJ, Gainetdinov RR and Caron MG (2005) An Akt/beta-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. Cell 122(2):261-273.

Biederman J and Faraone SV (2005) Attention-deficit hyperactivity disorder. Lancet 366(9481):237-248.

Kalivas PW and Volkow ND (2005) The neural basis of addiction: a pathology of motivation and choice. Am J Psychiatry 162(8):1403-1413.

Kim OJ, Ariano MA, Namkung Y, Marinec P, Kim E, Han J and Sibley DR (2008) D(2) dopamine receptor expression and trafficking is regulated through direct interactions with ZIP. J Neurochem.

Lachowicz JE and Sibley DR (1997) Molecular characteristics of mammalian dopamine receptors. Pharmacol Toxicol 81(3):105-113.

Liu XY, Chu XP, Mao LM, Wang M, Lan HX, Li MH, Zhang GC, Parelkar NK, Fibuch EE, Haines M, Neve KA, Liu F, Xiong ZG and Wang JQ (2006) Modulation of D2R-NR2B interactions in response to cocaine. Neuron 52(5):897-909.

Liu Y, Buck DC, Macey TA, Lan H and Neve KA (2007) Evidence that calmodulin binding to the dopamine D2 receptor enhances receptor signaling. J Recept Signal Transduct Res 27(1):47-65.

Macey TA, Gurevich VV and Neve KA (2004) Preferential Interaction between the dopamine D2 receptor and Arrestin2 in neostriatal neurons. Mol Pharmacol 66(6):1635-1642.

Missale C, Nash SR, Robinson SW, Jaber M and Caron MG (1998) Dopamine receptors: from structure to function. Physiological Reviews 78(1):189-225.

Negyessy L and Goldman-Rakic PS (2005) Subcellular localization of the dopamine D2 receptor and coexistence with the calcium-binding protein neuronal calcium sensor-1 in the primate prefrontal cortex. J Comp Neurol 488(4):464-475.

Neve KA, Seamans JK and Trantham-Davidson H (2004) Dopamine receptor signaling. J Recept Signal Transduct Res 24(3):165-205.

Rashid AJ, So CH, Kong MM, Furtak T, El-Ghundi M, Cheng R, O'Dowd BF and George SR (2007) D1-D2 dopamine receptor heterooligomers with unique pharmacology are coupled to rapid activation of Gq/11 in the striatum. Proc Natl Acad Sci U S A 104(2):654-659.

Smith FD, Oxford GS and Milgram SL (1999) Association of the D2 dopamine receptor third cytoplasmic loop with spinophilin, a protein phosphatase-1-interacting protein. J Biol Chem 274(28):19894-19900.

So CH, Varghese G, Curley KJ, Kong MM, Alijaniaram M, Ji X, Nguyen T, O'Dowd B F and George SR (2005) D1 and D2 dopamine receptors form heterooligomers and cointernalize after selective activation of either receptor. Mol Pharmacol 68(3):568-578.

Anmerkungen

Found in the "Discussion"-part of Amh's thesis. Not marked as a citation.

The references for "Liu et al., 2007" and "Neve et al., 2004" is missing from Amh.

Sichter
(Graf Isolan) Schumann

[19.] Amh/Fragment 024 03 - Diskussion
Bearbeitet: 7. May 2014, 13:39 Schumann
Erstellt: 7. May 2014, 06:41 (DerFurz)
Amh, Fragment, Gesichtet, Noble 2003, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
Verschleierung
Bearbeiter
DerFurz, Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 24, Zeilen: 3-20
Quelle: Noble 2003
Seite(n): 113, Zeilen: l.col: 44ff
A huge amount of data suggests that dopaminergic activation is a primary pathophysiologic component in certain subtypes of migraine (Peroutka, 1997). This has led to an examination of D2 variants in this disorder. In one study the NcoI D2 C to T polymorphism located in exon 6 was assessed in individuals having migraine with aura and without aura (Peroutka, 1997). Individuals having migraine with aura had a significantly higher frequency of the D2 C allele than did control or migraine without aura individuals. No D2 C allele frequency difference was found, however, between the latter two groups. The association of NcoI DRD2 variants in comorbid migraine with aura, anxiety and depression was also reported (Peroutka, 1998). The D2 C allele frequency was significantly higher in individuals with migraine without aura, anxiety disorders or major depression than in individuals who had none of these disorders. Another group (Del Zompo et al.,1998) utilized the Transmission Disequilibrium Test and the dinucleotide repeat alleles within intron 2 of the D2 gene to test for association with patients affected by migraine without aura. Although no difference was observed in D2 repeat allelic distribution in the overall sample, allelic distribution differed significantly in a subgroup of dopaminergic migraineurs. Another D2 gene polymorphism (promoter -141C Ins/Del), however, was not found to be associated with migraine (Maude et al., 2001). Furthermore, a significant and independent association was found of SNPs in the insulin receptor and the D2 SNP93 with migraine subjects (McCarthy et al., 2001). A growing body of data suggests that dopaminergic activation is a primary pathophysiologic component in certain subtypes of migraine [Peroutka, 1997]. This has led to an examination of DRD2 variants in this disorder. In one study [Peroutka et al., 1997], the NcoI DRD2 C to T polymorphism located in exon 6 was assessed in individuals having migraine with aura (MWA) and without aura (MO). Individuals having MWA had a significantly higher frequency of the DRD2 C allele than did controls or MO individuals. No DRD2 C allele frequency difference was found, however, between the latter two groups. The same laboratory [Peroutka et al., 1998] also studied the association of NcoI DRD2 variants in comorbid migraine with aura, anxiety and depression. The DRD2 C allele frequency was significantly higher in individuals with MWA, anxiety disorders or major depression than in individuals who had none of these disorders. Another group [Del Zompo et al., 1998] utilized the Transmission Disequilibrium Test and the dinucleotide repeat alleles within intron 2 of the DRD2 gene to test for association with patients affected by migraine without aura. Although no difference was observed in DRD2 repeat allelic distribution in the overall sample, allelic distribution differed significantly in a subgroup of dopaminergic migraineurs. Another DRD2 gene polymorphism (promoter 141C Ins/Del), however, was not found to be associated with migraine [Maude et al., 2001]. Finally, in a large study of subjects with typical migraine and controls, a significant and independent association was found of SNPs in the insulin receptor and the DRD2 SNP93 (NcoI polymorphism) with migraine subjects [McCarthy et al., 2001].
Anmerkungen

The source is mentioned in the previous paragraph, but without indication that the here documented paragraph is taken from it.

Sichter
(Hindemith) Schumann

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