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Autor     Anna Maria Haarmann
Titel    The effects of dopamine receptors on spreading depression in rat neocortical tissues
Ort    Münster
Jahr    2009
Anmerkung    Inaugural-Dissertation zur Erlangung des doctor medicinae der Medizinischen Fakultät der Westfälischen Wilhelms-Universität Münster, Tag der mündlichen Prüfung: 20.11.2009, online publication: 13.1.2010
URL    http://miami.uni-muenster.de/servlets/DocumentServlet?id=5056&XSL.H_main=S_GLOBAL&XSL.H_searchId=searchId

Literaturverz.   

no
Fußnoten    no
Fragmente    11


Fragmente der Quelle:
[1.] Clm/Fragment 017 08 - Diskussion
Zuletzt bearbeitet: 2014-05-08 21:25:48 Singulus
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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. Direct alterations of electrical activity of cortical neurons by the locally spreading wave can lead to clinical symptoms (e.g. the aura phase of migraine). The most common symptoms in aura phase are visual arising from dysfunction of occipital lobe neurons. The excitatory neurological symptoms, e.g., flashing lights are usually followed by suppressive ones, e.g., scotoma or hemianopia in this phase. Magnetoencephalographic studies in human noted that the magnetic signals were seen in migraineous 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 CSD 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.] [page 8]

Direct alterations of electrical activity of cortical neurons by the locally spreading wave can lead to clinical symptoms (e.g. the aura phase of migraine).

[page 9]

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.

Anmerkungen

No source given, nothing has been marked as a citation.

Sichter
(Graf Isolan) Schumann

[2.] Clm/Fragment 018 01 - Diskussion
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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 (Hadjikhani et al., 2001). Recent investigations provide early insights into mechanisms that lead to trigeminovascular activation.

Hadjikhani N, Sanchez Del Rio M, Wu O, Schwartz D, Bukker D, Fischt B, Kwong KK, Cutrer FM, Rosen BR, Tootell RB, Sorensen AG, Moskowitz MA. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc. Natl. Acad. Sci. USA., 2001;98:4687 4692.

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.

Recent investigations provide early insights into mechanisms that lead to trigeminovascular activation.

Anmerkungen

Nothing has been marked as a citation. A reference not appearing in the original text has been added.

Sichter
(Graf Isolan) Schumann

[3.] Clm/Fragment 018 19 - Diskussion
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Consistent with an upstream role for CSD, prolonged application of migraine prophylactic drugs suppresses CSD in experimental models as a proposed mechanism of action. In line with clinical recognition that prolonged administration of prophylactic medicaments is important to achieve maximum therapeutic efficacy, treatment extension beyond 3–4 weeks also maximizes the inhibitory effects of drugs such as topiramate, valproate, methysergide, amitriptyline, and propranolol (Gorji, 2001). 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.
Anmerkungen

Note: the passage cannot be found in this wording in Gorji (2001).

The source is not given.

Sichter
(Schumann), Hindemith

[4.] Clm/Fragment 020 01 - Diskussion
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Material and methods

The experiments were performed on adult rat (200-350g) somatosensory neocortical slices. The brain was removed under deep methohexital anaesthesia and placed in cold (1–4°C) artificial cerebrospinal fluid (ACSF) pre-equilibrated with 5% CO2 in O2 to give a pH of 7.4. The ACSF contained (in mM): NaCl 124, KCl 4, CaCl2 1.0, NaH2PO4 1.24, MgSO4 1.3, NaHCO3 26 and glucose 10. The somatosensory neocortices were dissected and cut into slices of 500 μm thickness. The slices were incubated in ACSF solution for >1 h at 28°C. After 30-min incubation, CaCl2 was elevated to 2.0 mM. Slices were transferred to an interphase-type experimental chamber and superfused with ACSF at 32°C (1.5–2 ml/min).

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.

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 μm; injection pressure 0.5–1.0 bar applied for 200–300 ms, two injections, 1–3 nl per pulse). 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.]

Material and methods

The experiments were performed on adult rat (250-350g) somatosensory neocortical slices. The brain was removed under deep methohexital anaesthesia and placed in cold (1–4°C) artificial cerebrospinal fluid (ACSF) pre-equilibrated with 5% CO2 in O2 to give a pH of 7.4. The ACSF contained (in mM): NaCl 124, KCl 4, CaCl2 1.0, NaH2PO4 1.24, MgSO4 1.3, NaHCO3 26 and glucose 10. The somatosensory neocortices were dissected and cut into slices of 500 μm thickness. The slices were incubated in ACSF solution for >1 h at 28°C. After 30-min incubation, CaCl2 was elevated to 2.0 mM. Slices were transferred to an interphase-type experimental chamber and superfused with ACSF at 32°C (1.5–2 ml/min).

Electrophysiological recordings

Extracellular field potentials were recorded with glass microelectrodes (150 mmol/l NaCl; 2–10 M ) 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.

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 μm; injection pressure 0.5–1.0 bar applied for 200–300 ms, two injections, 1–3 nl per pulse). 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.

Anmerkungen

Though identical, nothing has been marked as a citation.

Sichter
(Graf Isolan) Schumann

[5.] Clm/Fragment 021 01 - Diskussion
Zuletzt bearbeitet: 2014-05-09 18:36:45 Singulus
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[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 electrodes. Evoked field excitatory postsynaptic potentials (fEPSP) were recorded in the third layer of neocortical slices. The fEPSP was elicited by adjusting the intensity of stimulation to 50% of that at which population spikes after fEPSP began to appear. 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.

Experimental protocols

The experimental protocol consisted of four periods as follows: (a) control period, neocortical slices were superfused with ACSF (30 min), tested for spontaneous CSD; (b) KCl injection, induction of SD (CSD1); (c) application of garlic oil (1-500 μl/l) before the second injection of KCl (CSD2); (d) washout of garlic oil with ASCF (45 min, second control period), third injection of KCl (CSD3). Only a single concentration of garlic oil was used in a given slice.

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

[page 14]

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

Experimental protocols

The experimental protocol consisted of four periods as follows: (a) control period, neocortical slices were superfused with ACSF (30 min), tested for spontaneous SD; (b) KCl injection, induction of SD (SD1); (c) application of D2 dopamine receptor agonist quinpirole (10-200 μM), or the dopamine D2 dopamine receptor antagonist sulpiride (0.1-10 μM, 60 min) before the second injection of KCl (SD2); (d) washout of quinpirole or sulpiride with ASCF (45 min, second control period), third injection of KCl (SD3). Only a single concentration of quinpirole or sulpiride was used in a given slice

Anmerkungen

The source is not given.

Sichter
(Hindemith) Agrippina1

[6.] Clm/Fragment 022 03 - Diskussion
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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. Multiple comparisons were performed by analysis of variance test (ANOVA) for repeated measures followed by a Dunn’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 Holm-Sidak’s test. Significance was established when the probability values were less than 0.05. The investigations were approved

[page 15]

by the local ethics committee (Tierversuchsgenehmigung, Bezirksregierung Münster, Deutschland, AZ: 50.0835.1.0, G79/2002).

Anmerkungen

The source is not given.

Sichter
(Hindemith) Agrippina1

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Focal application of KCl in the sixth layer of neocortical tissues induced negative DC deflections followed by positive waves (amplitude of 14.7 ± 2.2 mV; duration of 121 ± 6 sec). Negative DC-fluctuations were sometimes preceded by small positive waves. These cortical CSD waves propagated opposite to the direction of the ACSF flow at propagation velocity of 3.3 ± 0.1 mm / min. The effect of five different concentrations of garlic oil (1, 10, 100, 500 μl/l; n = 6 for each concentration) was tested on potassium-evoked CSD in neocortical slices. The ratio between the second and the first DC potential waves (SD2/SD1) was calculated in slices treated with garlic oil. Focal application of KCl in the sixth layer of neocortical tissues induced negative DC deflections followed by positive waves (amplitude of 15.6 ± 1.9 mV; duration of 113 ± 5 sec). Negative DC-fluctuations were sometimes preceded by small positive waves. These cortical SD waves propagated opposite to the direction of the ACSF flow at propagation velocity of 3.1 ± 0.1 mm / min. The effect of five different concentrations of D2 dopamine receptor agonist quinpirole (10, 20, 50, 100, 200 μΜ; n = 6 for each concentration) was tested on potassium-evoked SD in neocortical tissues. The ratio between the second and the first DC potential waves (SD2/SD1) was calculated in control slices and slices treated with quinpirole.
Anmerkungen

Different experiment and different results, but the same text -- and the source is not given.

Sichter
(Hindemith) Schumann

[8.] Clm/Fragment 025 08 - Diskussion
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A conditioning tetanic stimulation was delivered to the white substance of neocortical slices followed by pulses with stimulation parameters identical to control values. The evoked fEPSP was stable for at least 30 min before application of tetanic stimulation (less than 10% variation; Fig. 4). Administration of tetanic stimulation produced a rapid and stable enhancement of the amplitude of the fEPSP in all tested preparations (n = 7, 154 ± 11 % control; Fig. 4). LTP lasted as long as the fEPSP were recorded (at least for 90 min). The potentiation rose within 1–2 min and stabilized within 5 minutes after the train of stimulations. Application of garlic oil (500μl/l; n = 12) sixty min before tetanic stimulation significantly suppressed LTP induction in all tested slices (134 ± 6 % baseline, Mann–Whitney Rank Sum test; P ≤ 0.001, Fig. 4). A conditioning tetanic stimulation was delivered to the white substance of neocortical slices followed by pulses with stimulation parameters identical to control values. The evoked fEPSP was stable for at least 30 min before application of tetanic stimulation (less than 10% variation; Fig. 6). Administration of tetanic stimulation produced a rapid and stable enhancement of the amplitude of the fEPSP in all tested preparations (n = 6, 164 ± 12 % control; Fig. 6). LTP lasted as long as the fEPSP were recorded (at least for 90 min). The potentiation rose within 1–2 min and stabilized within 5 minutes after the train of stimulations. Application of sulipride (5 μM; n = 10) sixty min before tetanic stimulation significantly suppressed LTP induction in all tested slices (122 ± 3 % baseline, Mann– Whitney Rank Sum test; P ≤ 0.001, Fig. 6). However, Application of quinpirole (50 μM; n = 10) sixty min before tetanic stimulation did not significantly change the LTP induction in compare with control tissues (147 ± 6 % baseline, Mann–Whitney Rank Sum test; P = 0.08, Fig. 6).
Anmerkungen

The source is not given, although it provided the structure and much of the text for the presentation of different results.

Sichter
(Hindemith) Singulus

[9.] Clm/Fragment 027 01 - Diskussion
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[B: Tetanic stimulation (Ten trains of four pulses;] pulse duration 0.1 msec; interpulse interval 50 msec; intensity 5 V) produces a rapid and stable potentiation in the amplitude of the evoked field potentials, calculated as a percentage of baseline mean response amplitude. Closed triangel and closed circles show the evoked fEPSP after application of garlic oil (500μl/l) and control, respectively. Arrow shows the time of tetanic stimulation, 60 min after application of substances. Application of garlic oil significantly inhibited LTP of the evoked field potentials (Mann–Whitney Rank Sum test, P = 0.001), calculated as a percentage of baseline mean response amplitude. [Page 21]

(A) Tetanic stimulation (Ten trains of four pulses; pulse duration 0.1 msec; interpulse interval 50 msec; intensity 5 V)) produces a rapid and stable potentiation in the amplitude of the evoked field potentials, calculated as a percentage of baseline mean response amplitude. Open triangles, open square, and closed circles show the evoked fEPSP after application of sulipride (5 μmol/l), quinpirole

[Page 22]

(50 μmol/l) and control, respectively. Arrow shows the time of tetanic stimulation, 60 min after application of substances. Application of sulipride significantly inhibited LTP of the evoked field potentials (Mann–Whitney Rank Sum test, P = 0.001), calculated as a percentage of baseline mean response amplitude.

Anmerkungen

Not marked as a citation.

Sichter
(Graf Isolan) Agrippina1

[10.] Clm/Fragment 029 01 - Diskussion
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LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting changes of which individual synapses are capable (Collingridge & Singer 1990, Malenka and Bear 2004). LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting modifications of which individual synapses are capable (Collingridge & Singer 1990, Malenka & Bear 2004).
Anmerkungen

As two sources are given this cannot be a quote from one of the two.

The source is not given.

Sichter
(Hindemith)

[11.] Clm/Fragment 030 04 - Diskussion
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CSD induces an LTP-like effect in rat neocortical slices (Footitt and Newberry, 1998) and enhances LTP induction in human neocortical tissues (Berger et al., 2008). SD induces an LTP-like effect in rat neocortical slices (Footitt and Newberry 1998) and enhances LTP induction in human neocortical tissues (Berger et al., 2008).
Anmerkungen

The source is not given.

Sichter
(Hindemith)

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