20 gesichtete, geschützte Fragmente: Plagiat
| [1.] Sng/Fragment 015 01 - Diskussion Bearbeitet: 9. May 2016, 20:05 WiseWoman Erstellt: 2. January 2014, 17:45 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 15, Zeilen: 1ff (komplett) |
Quelle: Sajikumar 2005 Seite(n): 14-15, 16, Zeilen: 14:15-24 - 15:1-2; 16:1-12 |
|---|---|
| 1.3.2. Hippocampus, an ideal structure for investigating synaptic plasticity
Hippocampus is one of the useful structures for brain slice preparation and for investigating synaptic plasticity. The main reason is because of its structure, that allows a slice to be cut whilst preserving a large number of neurons and their interconnecting axons (Andersen et al., 1969;Amaral and Witter, 1989). The dendritic structure of the three main hippocampal cell types and their interconnecting axons lay in a single plane. This plane is oriented normal to the ventricular surface and to the longitudinal axis of the hippocampus. The lamellar structure allows slices to be taken without destroying the neurons together with their dendrites and axons. The highly organized and laminar arrangement of synaptic pathways with its extensive connections makes the hippocampus (Fig.1, adapted from (Amaral and Witter, 1989)) a convenient model for studying synaptic function in vitro and in vivo (Andersen et al., 1969;Amaral and Witter, 1989). Brain slices offer a variety of novel opportunities, the most obvious being visual inspection. Depending upon the brain region, histological landmarks can be seen with an ordinary dissecting microscope. In many ways the tissue can be seen in a gross microscopic slide. This allows visual control of electrode placement. It is also possible to direct electrodes to known parts of a given cell. For example, in the hippocampus, an electrode may be placed in the apical or basal dendritic tree of pyramidal cells at known distances from the soma to record the activity of a small group of synapses. Hippocampal slices in vitro also allow a comparison of the effectiveness of proximal and distal synapses to the same cell to be made. A great advantage is the lack of anaesthesis. This is of obvious importance for many studies on neuronal excitability, [but is also invaluable for many pharmacological studies.] 11. Amaral DG, Witter MP (1989) The three-dimensional organization of the hippocampal formation: a review of anatomical data. Neuroscience 31: 571-591. 12. Andersen P, Bliss TV, Lomo T, Olsen LI, Skrede KK (1969) Lamellar organization of hippocampal excitatory pathways. Acta Physiol Scand 76: 4A-5A. |
[Seite 14]
Hippocampus is one of the useful structures for brain slice preparation and for investigating synaptic plasticity. The main reason is because of its structure, that allows a slice to be cut whilst preserving a large number of neurons and their interconnecting axons (Andersen et al., 1969;Amaral and Witter, 1989). The dendritic structure of the three main hippocampal cell types and their interconnecting axons lay in a single plane. This plane is oriented normal to the ventricular surface and to the longitudinal axis of the hippocampus. The lamellar structure allows slices to be taken without destroying the neurons together with their dendrites and axons. The highly organized and laminar arrangement of synaptic pathways [Seite 15] makes the hippocampus a convenient model for studying synaptic function in vivo and in vitro (Andersen et al., 1969;Amaral and Witter, 1989). [Seite 16] Brain slices offer a variety of novel opportunities, the most obvious being visual inspection. Depending upon the brain region, histological landmarks can be seen with an ordinary dissecting microscope. In many ways the tissue can be seen in a gross microscopic slide. This allows visual control of electrode placement. It is also possible to direct electrodes to known parts of a given cell. For example, in the hippocampus, an electrode may be placed in the apical or basal dendritic tree of pyramidal cells at known distances from the soma to record the activity of a small group of synapses. Hippocampal slice also allows a comparison of the effectiveness of proximal and distal synapses to the same cell to be made. A great advantage is the lack of anaesthesis. This is of obvious importance for many studies on neuronal excitability, but is also invaluable for many pharmacological studies. Amaral DG, Witter MP (1989) The three-dimensional organization of the hippocampal formation: a review of anatomical data. Neuroscience 31: 571-591. Andersen P, Bliss TV, Lomo T, Olsen LI, Skrede KK (1969) Lamellar organization of hippocampal excitatory pathways. Acta Physiol Scand 76: 4A-5A. |
Ohne Hinweis auf eine Übernahme. |
|
| [2.] Sng/Fragment 016 01 - Diskussion Bearbeitet: 22. May 2016, 21:31 Schumann Erstellt: 2. January 2014, 18:30 (Graf Isolan) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 16, Zeilen: 1-7 |
Quelle: Sajikumar 2005 Seite(n): 16, Zeilen: 13-20 |
|---|---|
| Furthermore, in the slice preparation, the influence of the blood brain barrier is removed. The ability to change the tissue concentration of interesting molecules at will provides good experimental control of the preparation. In addition to the temperature and oxygen concentration, the pH, ionic concentration and hormonal levels can be changed at will. The slice neurons are consequently under less synaptic bombardment than cells in the intact brain. Other modulating influences (neuromodulators, biological clocks, hormones) are also absent. | Furthermore, in the slice preparation the influence of the blood brain barrier is removed. The ability to change the tissue concentration of interesting molecules at will provides good experimental control of the preparation. In addition to the temperature and oxygen concentration, the pH, ionic concentration and hormonal levels can be changed at will. The slice neurons are consequently under less synaptic bombardment than cells in the intact brain. Other modulating influences (neuromodulators, biological clocks, hormones) are also absent. |
Ohne Hinweis auf eine Übernahme. |
|
| [3.] Sng/Fragment 016 16 - Diskussion Bearbeitet: 22. May 2016, 21:34 Schumann Erstellt: 2. January 2014, 21:03 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 16, Zeilen: 16-23 |
Quelle: Sajikumar 2005 Seite(n): 12, Zeilen: 1-10 |
|---|---|
| Hebb (1949) increased our understanding of how networks of neurons might store information with the provocative theory that memories are represented by reverberating assemblies of neurons. Hebb recognized that a memory so represented cannot reverberate forever and that some alteration in the network must occur to provide integrity both to make the assembly a permanent trace and to make it more likely that the trace could be reconstructed as a remembrance. Neurons communicate with each other only at synapses, the activity of the assembly or network is most easily altered by changes in synaptic function. | Hebb (Hebb, 1949) increased our understanding of how networks of neurons might store information with the provocative theory, that memories are represented by reverberating assemblies of neurons. Hebb recognized that a memory, so represented cannot reverberate forever and that some alteration in the network must occur, to provide integrity both to make the assembly a permanent trace and to make it more likely that, the trace could be reconstructed as a remembrance. Because neurons communicate with each other mainly through synapses, the activity of the assembly or network is most easily (perhaps only) altered by changes in synaptic function.
Hebb DO (1949). The Organization of Behavior. New York: Wiley (Interscience), 62, 70. |
Ohne Hinweis auf eine Übernahme. Hebb (1949) wird in Sng nicht aufgeschlüsselt. |
|
| [4.] Sng/Fragment 019 07 - Diskussion Bearbeitet: 22. May 2016, 21:41 Schumann Erstellt: 4. January 2014, 13:07 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 19, Zeilen: 7-23 |
Quelle: Sajikumar 2005 Seite(n): 19, Zeilen: 3-22 |
|---|---|
| 1.5.1. Multiple Phases of LTP and LTD
Brief high-frequency stimulation of the CA3-CA1 synapses can result in LTP, which can be divided into several temporal phases characterized by different underlying mechanisms. In general, it is divided into induction, expression and maintenance. The initial induction phase of LTP i.e. so named ‘posttetanic potentiation’ (PTP) with a duration of several seconds to minutes is characterized by presynaptic mechanisms, i.e. transient increase in transmitter release. PTP is followed by a ‘short-term potentiation’ (STP) with a duration up to one hour. Postsynaptic events like activation of transmitter receptors by local protein kinases (e.g. CaMKII, tyrosine kinase) (Dobrunz et al., 1997;Huang, 1998) are responsible for the maintenance of that phase. STP can be followed by at least two further phases: early-and late-LTP (Matthies et al., 1990;Huang, 1998). Early-LTP is a transient form of LTP which lasts 2-3 h in vitro and 7-8 h in vivo, while late-LTP lasts for 8-10 h in vitro and days or even months in intact animals (Abraham and Bear, 1996;Abraham, 2003) (Fig. 2). The different forms of LTP can be specifically induced by distinct stimulus protocols in acute slices in vitro (Frey et al., 1993;Huang and Kandel, 1994). A single high-frequency stimulus train of distinct stimulation strength can induce early-LTP, but [such a protocol is normally not sufficient to induce late-LTP.] 1. Abraham WC (2003) How long will long-term potentiation last? Philos Trans R Soc Lond B Biol Sci 358: 735-744. 2. Abraham WC, Bear MF (1996) Metaplasticity: the plasticity of synaptic plasticity. Trends Neurosci 19: 126-130. 40. Dobrunz LE, Huang EP, Stevens CF (1997) Very short-term plasticity in hippocampal synapses. Proc Natl Acad Sci U S A 94: 14843-14847. 54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. 71. Huang EP (1998) Synaptic plasticity: going through phases with LTP. Curr Biol 8: R350-R352. 72. Huang YY, Kandel ER (1994) Recruitment of long-lasting and protein kinase A-dependent long-term potentiation in the CA1 region of hippocampus requires repeated tetanization. Learn Mem 1: 74-82. 103. Matthies H, Frey U, Reymann K, Krug M, Jork R, Schroeder H (1990) Different mechanisms and multiple stages of LTP. Adv Exp Med Biol 268:359-68.: 359-368. |
1.3. Temporal phases of LTP and LTD
Brief high-frequency stimulation of the the [sic] CA3-CA1 synapses can result in LTP, which can be divided into several temporal phases characterized by different underlying mechanisms. In general, it is divided into induction, expression and maintenance. The initial induction phase of LTP i.e. so named ‘posttetanic potentiation’ (PTP) with a duration of several seconds to minutes is characterized by presynaptic mechanisms, i.e. transient increase in transmitter release (Huang, 1998;Dobrunz et al., 1997). PTP is followed by a ‘short-term potentiation’ (STP) with a duration up to one hour. Postsynaptic events like activation of receptors by local protein kinases (e.g. CaMKII, tyrosine kinase) (Huang, 1998;Dobrunz et al., 1997) are responsible for the maintenance of that phase. STP can be followed by at least two further phases: early-and late-LTP (Matthies et al., 1990;Huang, 1998). Early-LTP is a transient form of LTP which lasts 3-4 h in vitro and 7-8 h in vivo, while late-LTP lasts for 8-10 h in vitro and days or even months in intact animals The different forms of LTP can be specifically induced by distinct stimulus protocols in acute slices in vitro (Frey et al., 1993;Huang and Kandel, 1994). A single high-frequency stimulus train of distinct stimulation strength can induce early-LTP that lasts for up to 3-4 h, but such a protocol is normally not sufficient to induce late-LTP. Dobrunz LE, Huang EP, Stevens CF (1997) Very short-term plasticity in hippocampal synapses. Proc Natl Acad Sci U S A 94: 14843-14847. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. Huang EP (1998) Synaptic plasticity: going through phases with LTP. Curr Biol 8: R350-R352. Huang YY, Kandel ER (1994) Recruitment of long-lasting and protein kinase A-dependent long-term potentiation in the CA1 region of hippocampus requires repeated tetanization. Learn Mem 1: 74-82. Matthies H, Frey U, Reymann K, Krug M, Jork R, Schroeder H (1990) Different mechanisms and multiple stages of LTP. Adv Exp Med Biol 268:359-68.: 359-368. |
Ohne Hinweis auf eine Übernahme trotz Übereinstimmung bis in kleinste Details. |
|
| [5.] Sng/Fragment 020 01 - Diskussion Bearbeitet: 22. May 2016, 21:42 Schumann Erstellt: 4. January 2014, 13:44 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 20, Zeilen: 1ff (komplett) |
Quelle: Sajikumar 2005 Seite(n): 19-20, Zeilen: 19:22-23 - 20:1-13 - 21:1-3 |
|---|---|
| The induction of late-LTP, on the other hand, requires repeated or stronger trains of high-frequency stimulation. Processes specifically involved in early- and late- phases of LTP require different cellular signaling pathways.
[Fig. 2. The multiple phases of LTP. See text for a detailed description.] The early-phase of LTP is transient and protein synthesis- independent induced by second messenger cascades, activated by Ca2+ influx, and maintained by activated kinases like CaMKII, tyrosine kinase, (Malenka and Nicoll, 1999;Soderling and Derkach, 2000). Late-LTP begins gradually during the first 2-3 h and can last for 6-10 h in hippocampal slices in vitro and for days to months in vivo (Krug et al., 1989;Frey et al., 1995;Otani and Abraham, 1989;Abraham et al., 2002;Kandel, 2001;Reymann et al., 1985). A further major difference between early-LTP and late-LTP is that late-LTP requires protein synthesis (Krug et al., 1984;Frey et al., 1988;Otani et al., 1989). Application of suppressors of RNA-translation during LTP-induction resulted in a [decremental early-LTP while late-LTP was prevented (Krug et al., 1984;Stanton and Sarvey, 1984;Deadwyler et al., 1987;Abraham and Kairiss, 1988;Frey et al., 1988;Frey et al., 1996;Mochida et al., 2001).] 3. Abraham WC, Kairiss EW (1988) Effects of the NMDA antagonist 2AP5 on complex spike discharge by hippocampal pyramidal cells. Neurosci Lett 89: 36-42. 4. Abraham WC, Logan B, Greenwood JM, Dragunow M (2002) Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. J Neurosci 22: 9626-9634. 36. Deadwyler SA, Dunwiddie T, Lynch G (1987) A critical level of protein synthesis is required for long-term potentiation. Synapse 1: 90-95. 52. Frey U, Frey S, Schollmeier F, Krug M (1996) Influence of actinomycin D, a RNA synthesis inhibitor, on long-term potentiation in rat hippocampal neurons in vivo and in vitro. J Physiol 490: 703-711. 55. Frey U, Krug M, Reymann KG, Matthies H (1988) Anisomycin, an inhibitor of protein synthesis, blocks late phases of LTP phenomena in the hippocampal CA1 region in vitro. Brain Res 452: 57-65. 60. Frey U, Schollmeier K, Reymann KG, Seidenbecher T (1995) Asymptotic hippocampal long-term potentiation in rats does not preclude additional potentiation at later phases. Neuroscience 67: 799-807. 81. Kandel ER (2001) The molecular biology of memory storage: a dialogue between genes and synapses. Science 294: 1030-1038. 90. Krug M, Koch M, Schoof E, Wagner M, Matthies H (1989) Methylglucamine orotate, a memory-improving drug, prolongs hippocampal long-term potentiation. Eur J Pharmacol 173: 223-226. 91. Krug M, Lossner B, Ott T (1984) Anisomycin blocks the late phase of long-term potentiation in the dentate gyrus of freely moving rats. Brain Res Bull 13: 39-42. 97. Malenka RC, Nicoll RA (1999) Long-term potentiation--a decade of progress? Science 285: 1870-1874. 107. Mochida H, Sato K, Sasaki S, Yazawa I, Kamino K, Momose-Sato Y (2001) Effects of anisomycin on LTP in the hippocampal CA1: long-term analysis using optical recording. Neuroreport 12: 987-991. 124. Otani S, Abraham WC (1989) Inhibition of protein synthesis in the dentate gyrus, but not the entorhinal cortex, blocks maintenance of long-term potentiation in rats. Neurosci Lett 106: 175-180. 125. Otani S, Marshall CJ, Tate WP, Goddard GV, Abraham WC (1989) Maintenance of long-term potentiation in rat dentate gyrus requires protein synthesis but not messenger RNA synthesis immediately post-tetanization. Neuroscience 28: 519-526. 133. Reymann KG, Malisch R, Schulzeck K, Brodemann R, Ott T, Matthies H (1985) The duration of long-term potentiation in the CA1 region of the hippocampal slice preparation. Brain Res Bull 15: 249-255. 150. Soderling TR, Derkach VA (2000) Postsynaptic protein phosphorylation and LTP. Trends Neurosci 23: 75-80. 155. Stanton PK, Sarvey JM (1984) Blockade of long-term potentiation in rat hippocampal CA1 region by inhibitors of protein synthesis. J Neurosci 4: 3080-3088. |
[Seite 19]
The induction of late-LTP, on the other hand, requires repeated or stronger trains of high-frequency stimulation. Processes [Seite 20] specifically involved in early- and late- phases of LTP require different cellular signaling pathways (Fig. 2). [Figure 2. The multiple phases of LTP. See text for a detailed description.] The early-phase of LTP is transient and protein synthesis- independent, lasting about 2-4 h, induced by second messenger cascades, activated by Ca2+ influx, and maintained by activated kinases like CaMKII, tyrosine kinase, (Malenka and Nicoll, 1999;Soderling and Derkach, 2000). Late-LTP begins gradually during the first 1-3 h and can last for 6-10 h in hippocampal slices in vitro and for days to months in vivo (Krug et al., 1989;Frey et al., 1995;Reymann et al., 1985;Otani et al., 1989;Abraham et al., 2002;Kandel, 2001). A further major difference between early-LTP and late-LTP is that late-LTP requires protein synthesis (Krug et al., 1984;Frey et al., 1988;Otani et al., 1989). Application of suppressors of RNA-translation during LTP-induction resulted in a decremental early-LTP while late-LTP was [Seite 21] prevented (Krug et al., 1984;Stanton and Sarvey, 1984;Deadwyler et al., 1987;Abraham and Kairiss, 1988;Frey et al., 1988;Frey et al., 1996;Mochida et al., 2001). Abraham WC, Kairiss EW (1988) Effects of the NMDA antagonist 2AP5 on complex spike discharge by hippocampal pyramidal cells. Neurosci Lett 89: 36-42. Abraham WC, Logan B, Greenwood JM, Dragunow M (2002) Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. J Neurosci 22: 9626-9634. Deadwyler SA, Dunwiddie T, Lynch G (1987) A critical level of protein synthesis is required for long-term potentiation. Synapse 1: 90-95. Frey U, Frey S, Schollmeier F, Krug M (1996) Influence of actinomycin D, a RNA synthesis inhibitor, on long-term potentiation in rat hippocampal neurons in vivo and in vitro. J Physiol 490: 703-711. Frey U, Krug M, Reymann KG, Matthies H (1988) Anisomycin, an inhibitor of protein synthesis, blocks late phases of LTP phenomena in the hippocampal CA1 region in vitro. Brain Res 452: 57-65. Frey U, Schollmeier K, Reymann KG, Seidenbecher T (1995) Asymptotic hippocampal long-term potentiation in rats does not preclude additional potentiation at later phases. Neuroscience 67: 799-807. Kandel ER (2001) The molecular biology of memory storage: a dialogue between genes and synapses. Science 294: 1030-1038. Krug M, Koch M, Schoof E, Wagner M, Matthies H (1989) Methylglucamine orotate, a memory-improving drug, prolongs hippocampal long-term potentiation. Eur J Pharmacol 173: 223-226. Krug M, Lossner B, Ott T (1984) Anisomycin blocks the late phase of long-term potentiation in the dentate gyrus of freely moving rats. Brain Res Bull 13: 39-42. Malenka RC, Nicoll RA (1999) Long-term potentiation--a decade of progress? Science 285: 1870-1874. Mochida H, Sato K, Sasaki S, Yazawa I, Kamino K, Momose-Sato Y (2001) Effects of anisomycin on LTP in the hippocampal CA1: long-term analysis using optical recording. Neuroreport 12: 987-991. Otani S, Abraham WC (1989) Inhibition of protein synthesis in the dentate gyrus, but not the entorhinal cortex, blocks maintenance of long-term potentiation in rats. Neurosci Lett 106: 175-180. Otani S, Marshall CJ, Tate WP, Goddard GV, Abraham WC (1989) Maintenance of long-term potentiation in rat dentate gyrus requires protein synthesis but not messenger RNA synthesis immediately post-tetanization. Neuroscience 28: 519-526. Reymann KG, Malisch R, Schulzeck K, Brodemann R, Ott T, Matthies H (1985) The duration of long-term potentiation in the CA1 region of the hippocampal slice preparation. Brain Res Bull 15: 249-255. Soderling TR, Derkach VA (2000) Postsynaptic protein phosphorylation and LTP. Trends Neurosci 23: 75-80. Stanton PK, Sarvey JM (1984) Blockade of long-term potentiation in rat hippocampal CA1 region by inhibitors of protein synthesis. J Neurosci 4: 3080-3088. |
Ohne Hinweis auf eine Übernahme. "Figure 2" ist ebenfalls identisch. |
|
| [6.] Sng/Fragment 023 04 - Diskussion Bearbeitet: 22. May 2016, 22:02 Schumann Erstellt: 6. January 2014, 23:36 (Graf Isolan) | Fragment, Gesichtet, KomplettPlagiat, Makhinson et al 1999, SMWFragment, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 23, Zeilen: 4-16 |
Quelle: Makhinson et al 1999 Seite(n): 2507-2508, Zeilen: 2507:re.Sp. 47-62 - 2508:li.Sp. 1-2 |
|---|---|
| The Lisman model of LTP (Lisman and McIntyre, 2001) proposes that patterns of synaptic activity that produce low levels of NMDA receptor activation and small increase in intracellular Ca2+ depress synaptic strength via a cascade of protein phosphatase activation (Mulkey et al., 1993). This cascade of protein phosphatase activation is thought to entail a Ca2+- and calmodulin-dependent activation of calcineurin, that dephosphorylates the PP1 regulatory protein inhibitor-1 (Mulkey et al., 1994). Dephosphorylation of inhibitor-1 activates PP1 that in turn dephosphorylates CaMKII. In contrast, stronger levels of NMDA receptor activation and larger increase in intracellular Ca2+ induce LTP by increasing levels of autophosphorylated CaMKII via a simultaneous activation of CaMKII and downregulation of PP1. In the model, a large increase in Ca2+ is thought to suppress PP1 activation by stimulating Ca2+- and calmodulin-sensitive isoforms of adenylate cyclase (AC) and by activating PKA that suppresses PP1 activation by opposing calcineurin-mediated dephosphorylation of inhibitor-1.
94. Lisman JE, McIntyre CC (2001) Synaptic plasticity: a molecular memory switch. Curr Biol 11: R788-R791. 110. Mulkey RM, Endo S, Shenolikar S, Malenka RC (1994) Involvement of a calcineurin/inhibitor-1 phosphatase cascade in hippocampal long-term depression. Nature 369: 486-488. 111. Mulkey RM, Herron CE, Malenka RC (1993) An essential role for protein phosphatases in hippocampal long-term depression. Science 261: 1051-1055. |
[Seite 2507]
The Lisman model of LTP (Lisman, 1994) proposes that patterns of synaptic activity that produce low levels of NMDA receptor activation and small increases in intracellular Ca2+ depress synaptic strength via a cascade of protein phosphatase activation (Mulkey and Malenka, 1992; Mulkey et al., 1993, 1994). This cascade of protein phosphatase activation is thought to entail a Ca2+- and calmodulin-dependent activation of calcineurin that dephosphorylates the PP1 regulatory protein inhibitor-1 (Mulkey et al., 1994). Dephosphorylation of inhibitor-1 activates PP1 that in turn dephosphorylates CaMKII. In contrast, stronger levels of NMDA receptor activation and larger increases in intracellular Ca2+ induce LTP by increasing levels of autophosphorylated CaMKII via a simultaneous activation of CaMKII and downregulation of PP1. In the model, a large increase in Ca2+ is thought to suppress PP1 activation by stimulating Ca2+- and calmodulin-sensitive isoforms of AC and by [Seite 2508] activating PKA that suppresses PP1 activation by opposing calcineurin-mediated dephosphorylation of inhibitor-1. Lisman JE (1994) The CaM kinase II hypothesis for the storage of synaptic memory. Trends Neurosci 17:406–412. Mulkey RM, Malenka RC (1992) Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus. Neuron 9:967–975. Mulkey RM, Herron CE, Malenka RC (1993) An essential role for protein phosphatases in hippocampal long-term depression. Science 261:1051–1055. Mulkey RM, Endo S, Shenolikar A, Malenka RC (1994) Involvement of a calcineurin/inhibitor-1 phosphatase cascade in hippocampal longterm depression. Nature 369:486–488. |
Ohne Hinweis auf eine Übernahme. |
|
| [7.] Sng/Fragment 023 17 - Diskussion Bearbeitet: 22. May 2016, 22:04 Schumann Erstellt: 7. January 2014, 00:15 (Graf Isolan) | Blitzer et al 2005, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 23, Zeilen: 17-22 |
Quelle: Blitzer et al 2005 Seite(n): 114, Zeilen: re.Sp. 39-47 |
|---|---|
| A major target for Ca2+ is CaMKII, and among its many actions are the phosphorylation of GluR1 at serine 831 (which increases the channel conductance of the AMPA receptor; (Lee et al., 2000)), and the insertion of the receptor into the postsynaptic membrane through an indirect mechanism; (Hayashi et al., 2000). From a network perspective, the multiple effects of activated CaMKII define it as a ´node´, a point where a signal is split and directed to multiple targets (Schmitt et al., 2005).
66. Hayashi Y, Shi SH, Esteban JA, Piccini A, Poncer JC, Malinow R (2000) Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction. Science 287: 2262-2267. 92. Lee HK, Barbarosie M, Kameyama K, Bear MF, Huganir RL (2000) Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity. Nature 405: 955-959. 141. Schmitt JM, Guire ES, Saneyoshi T, Soderling TR (2005) Calmodulin-dependent kinase kinase/calmodulin kinase I activity gates extracellular-regulated kinase-dependent long-term potentiation. J Neurosci 25: 1281-1290. |
A major target for Ca2+ is Ca2+/calmodulin-dependent kinase type II (CaMKII), a major component of the postsynaptic density. Among its many actions are the phosphorylation of GluR1 at serine 831 (which increases the channel conductance of the AMPA receptor; Lee et al 2000), and the insertion of the receptor into the postsynaptic membrane (through an indirect mechanism; Hayashi et al 2000). From a network perspective, the multiple effects of activated CaMKII define it as a “node,” a point where a signal is split and directed to multiple targets.
Hayashi Y, Shi SH, Esteban JA, Piccini A, Poncer JC, Malinow R (2000): Driving AMPA receptors into synapses by LTP and CaMKII: Requirement for GluR1 and PDZ domain interaction. Science 287:2262–2267. Lee HK, Barbarosie M, Kameyama K, Bear MF, Huganir RL (2000): Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity. Nature 405:955–959. |
Ohne Hinweis auf eine Übernahme. |
|
| [8.] Sng/Fragment 024 01 - Diskussion Bearbeitet: 22. May 2016, 22:06 Schumann Erstellt: 7. January 2014, 00:42 (Graf Isolan) | Blitzer et al 2005, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 24, Zeilen: 1-12 |
Quelle: Blitzer et al 2005 Seite(n): 115, Zeilen: Legende zu Figure 2 |
|---|---|
| 1.6.3. The interaction of three major postsynaptic signaling pathways in LTP
Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3′,5′-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP (Frey et al., 1993;English and Sweatt, 1997;Bortolotto and Collingridge, 1998). The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation (Giovannini et al., 2001). PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase (Atkins et al., 2005). 15. Atkins CM, Davare MA, Oh MC, Derkach V, Soderling TR (2005) Bidirectional regulation of cytoplasmic polyadenylation element-binding protein phosphorylation by Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 1 during hippocampal long-term potentiation. J Neurosci 25: 5604-5610. 26. Bortolotto ZA, Collingridge GL (1998) Involvement of calcium/calmodulin-dependent protein kinases in the setting of a molecular switch involved in hippocampal LTP. Neuropharmacology 37: 535-544. 47. English JD, Sweatt JD (1997) A requirement for the mitogen-activated protein kinase cascade in hippocampal long term potentiation. J Biol Chem 272: 19103-19106. 54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. 64. Giovannini MG, Blitzer RD, Wong T, Asoma K, Tsokas P, Morrison JH, Iyengar R, Landau EM (2001) Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation. J Neurosci 21: 7053-7062. |
Figure 2. The interaction of three major postsynaptic signaling pathways in LTP. Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3’,5’-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP. The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases, and PKA can additionally be activated by β-adrenergic receptors (β-AR) and other G protein-coupled receptors. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation. PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase. |
Ohne Hinweis auf eine Übernahme. |
|
| [9.] Sng/Fragment 024 14 - Diskussion Bearbeitet: 22. May 2016, 22:05 Schumann Erstellt: 6. January 2014, 23:50 (Graf Isolan) | Fragment, Gesichtet, Makhinson et al 1999, SMWFragment, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 24, Zeilen: 14-21 |
Quelle: Makhinson et al 1999 Seite(n): 2508, Zeilen: li.Sp. 53-62 |
|---|---|
| Though PKA was initially identified as having an important signaling role in the protein synthesis-dependent late stages of LTP (Frey et al., 1993), more recent evidence suggests that PKA also provides a mechanism for suppression of protein phosphatase activation in the early stages of LTP induction (Blitzer et al., 1995;Winder et al., 1998;Blitzer et al., 1998). Activation of the cAMP-PKA signaling pathway regulates both activity-dependent changes in synaptic strength and CaMKII phosphorylation in a chemical LTP induction protocol (Yamamori et al., 2004).
23. Blitzer RD, Connor JH, Brown GP, Wong T, Shenolikar S, Iyengar R, Landau EM (1998) Gating of CaMKII by cAMP-regulated protein phosphatase activity during LTP. Science 280: 1940-1942. 24. Blitzer RD, Wong T, Nouranifar R, Iyengar R, Landau EM (1995) Postsynaptic cAMP pathway gates early LTP in hippocampal CA1 region. Neuron 15: 1403-1414. 54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. 171. Winder DG, Mansuy IM, Osman M, Moallem TM, Kandel ER (1998) Genetic and pharmacological evidence for a novel, intermediate phase of long-term potentiation suppressed by calcineurin. Cell 92: 25-37. 174. Yamamori E, Asai M, Yoshida M, Takano K, Itoi K, Oiso Y, Iwasaki Y (2004) Calcium/calmodulin kinase IV pathway is involved in the transcriptional regulation of the corticotropin-releasing hormone gene promoter in neuronal cells. J Mol Endocrinol 33: 639-649. |
Although PKA was initially identified as having an important signaling role in the protein synthesis-dependent late stages of LTP (Frey et al., 1993; Matthies and Reymann, 1993), more recent evidence suggests that PKA also provides a mechanism for suppression of protein phosphatase activation in the early stages of LTP induction (Blitzer et al., 1995, 1998; Thomas et al., 1996; Winder et al., 1998). Consistent with this notion, our results show that activation of the cAMP–PKA signaling pathway regulates both activity-dependent changes in synaptic strength and CaMKII phosphorylation in a chemLTP induction protocol.
Blitzer RD, Wong T, Nouranifar R, Iyengar R, Landau EM (1995) Postsynaptic cAMP pathway gates early LTP in the hippocampal CA1 region. Neuron 15:1403–1414. Blitzer RD, Connor JH, Brown GP, Wong T, Shenolikar S, Iyengar R, Landau EM (1998) Gating of CaMKII by cAMP-regulated protein phosphatase activity during LTP. Science 280:1940 –1943. Frey U, Huang Y-Y, Kandel ER (1993) Effects of cAMP simulate a late phase of LTP in hippocampal CA1 neurons. Science 260:1661–1664. Matthies H, Reymann KG (1993) Protein kinase A inhibitors prevent the maintenance of hippocampal long-term potentiation. NeuroReport 4:712–714. Thomas MJ, Moody TD, Makhinson M, O’Dell TJ (1996) Activity-dependent b-adrenergic modulation of low frequency stimulation induced LTP in the hippocampal CA1 region. Neuron 17:475– 482. Winder DG, Mansuy IM, Osman M, Moallem TM, Kandel ER (1998) Genetic and pharmacological evidence for a novel, intermediate phase of long-term potentiation suppressed by calcineurin. Cell 92:25–37. |
Ohne Hinweis auf eine Übernahme. |
|
| [10.] Sng/Fragment 028 14 - Diskussion Bearbeitet: 22. May 2016, 22:07 Schumann Erstellt: 14. January 2014, 20:06 (Graf Isolan) | Barad et al 1998, BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 28, Zeilen: 14-21 |
Quelle: Barad et al 1998 Seite(n): 15020, Zeilen: right col. 6-15 |
|---|---|
| The dependence of late-LTP, in hippocampal slices and behavioral memory, on PKA activity suggests that increasing cAMP signaling might increase behavioral memory by raising the probability that long-lasting synaptic plasticity would occur after synaptic stimulation (Barad et al., 1998). Administration of cAMP analogs such as Sp-cAMPS alone can cause long-lasting potentiation in rats that occludes subsequent electrical induction of late-LTP (Frey et al., 1993), suggesting that simply elevating cAMP throughout the hippocampus or brain might occlude rather than enhance synapse-specific strengthening.
16. Barad M, Bourtchouladze R, Winder DG, Golan H, Kandel E (1998) Rolipram, a type IV-specific phosphodiesterase inhibitor, facilitates the establishment of long-lasting long-term potentiation and improves memory. Proc Natl Acad Sci U S A 95: 15020-15025. 54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. |
The dependence of L-LTP, in hippocampal slices and behavioral memory, on PKA activity suggests that increasing cAMP signaling might increase behavioral memory by raising the probability that long-lasting synaptic plasticity would occur after synaptic stimulation. However, administration of cAMP analogs such as Sp-cAMPS alone can cause long-lasting potentiation in rats that occludes subsequent electrical induction of L-LTP (11), suggesting that simply elevating cAMP throughout the hippocampus or brain might occlude rather than enhance synapse-specific strengthening.
11. Frey, U., Huang, Y. Y. & Kandel, E. R. (1993) Science 260, 1661–1664. |
Art und Umfang der Übernahme bleiben ungekennzeichnet. |
|
| [11.] Sng/Fragment 034 15 - Diskussion Bearbeitet: 22. May 2016, 21:46 Schumann Erstellt: 5. January 2014, 10:09 (Graf Isolan) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 34, Zeilen: 15-23 |
Quelle: Sajikumar 2005 Seite(n): 35, Zeilen: 35:14-17.20-25 - 36:1. |
|---|---|
| As a possible solution to this targeting problem, the 'synaptic tag hypothesis' (Frey and Morris, 1997;Frey and Morris, 1998a) proposed that the persistence of LTP is mediated by the intersection of two dissociable events. The first event involves the generation of a local ‘synaptic tag’ at specific synapses in association with and perhaps causally related to the induction of LTP. The second involves the production and diffuse distribution of ‘plasticity-related proteins’ (PRPs) that are captured and utilised only at those synapses possessing a tag.
The ´synaptic tagging´ hypothesis describes a mechanism, how input specificity is achieved during a protein synthesis-dependent stage (Frey and Morris, 1997;Frey and Morris, 1998a;Frey and Morris, 1998b;Martin and Kosik, 2002). 57. Frey U, Morris RG (1997) Synaptic tagging and long-term potentiation. Nature 385: 533-536. 58. Frey U, Morris RG (1998a) Synaptic tagging: implications for late maintenance of hippocampal long-term potentiation. Trends Neurosci 21: 181-188. 59. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. 101. Martin KC, Kosik KS (2002) Synaptic tagging -- who's it? Nat Rev Neurosci 3: 813-820. |
[Seite 35]
The ´synaptic tagging´ hypothesis describes a mechanism, how input specificity is achieved during a protein synthesis-dependent stage (Frey and Morris, 1997;Frey and Morris, 1998a;Frey and Morris, 1998b;Martin and Kosik, 2002). [...] The synaptic tag hypothesis (Frey and Morris, 1997;Frey and Morris, 1998a) proposed that the persistence of LTP is mediated by the intersection of two dissociable events. The first event involves the generation of a local ‘synaptic tag’ at specific synapses in association with and perhaps causally related to the induction of LTP. The second involves the production and diffuse distribution of ‘plasticity related proteins’ (PRPs) that are captured and [Seite 36] utilized only at those synapses possessing a tag. Frey U, Morris RG (1997) Synaptic tagging and long-term potentiation. Nature 385: 533-536. Frey U, Morris RG (1998a) Synaptic tagging: implications for late maintenance of hippocampal long-term potentiation. Trends Neurosci 21: 181-188. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. Martin KC, Kosik KS (2002) Synaptic tagging -- who's it? Nat Rev Neurosci 3: 813-820. |
Ohne Hinweis auf eine Übernahme. Sng hat einfach die Reihenfolge der Absätze umgestellt; ansonsten erfolgt bis auf Auslassungen kein inhaltlicher Eingriff. |
|
| [12.] Sng/Fragment 035 01 - Diskussion Bearbeitet: 22. May 2016, 21:48 Schumann Erstellt: 5. January 2014, 13:06 (Graf Isolan) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 35, Zeilen: 1-8 |
Quelle: Sajikumar 2005 Seite(n): 36, Zeilen: 10-14, 17-21 |
|---|---|
| [Late-LTP was induced] on one pathway (S1), and the protein synthesis inhibitor anisomycin was then bath applied just before the second pathway (S2) was tetanised. Normally, only early-LTP would be induced and late-LTP inhibited in the presence of anisomycin. However, the LTP induced on S2 remained potentiated for up to 8 h post-tetanus. Similarly, “weak” tetanic stimulation that normally induces only early-LTP could be ‘transformed’ into late-LTP heterosynaptically if a “strong” tetanus was delivered to an independent input to the same population of CA1 pyramidal cells shortly before or shortly after the weak tetanus (Frey and Morris, 1998b).
59. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. |
Late-LTP was induced on one pathway (S1), and the protein synthesis inhibitor anisomycin then bath applied just before the second pathway (S2) was tetanised. Normally, only early-LTP would be induced and late-LTP inhibited in the presence of anisomycin. However, the LTP induced on S2 remained potentiated for up to 8 h post-tetanus (Frey and Morris, 1997).
[...] The weak tetanic stimulation that normally induces only early-LTP could be ‘transformed’ into late-LTP heterosynaptically if a strong tetanus was delivered to an independent input to the same population of CA1 pyramidal cells shortly before or shortly after the weak tetanus (Frey and Morris, 1998b). Frey U, Morris RG (1997) Synaptic tagging and long-term potentiation. Nature 385: 533-536. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. |
Ohne Hinweis auf eine Übernahme. |
|
| [13.] Sng/Fragment 038 01 - Diskussion Bearbeitet: 22. May 2016, 21:51 Schumann Erstellt: 14. January 2014, 20:24 (Graf Isolan) | Fragment, Gesichtet, Martin und Kosik 2002, SMWFragment, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 38, Zeilen: 1-10 |
Quelle: Martin und Kosik 2002 Seite(n): 815-816, Zeilen: 815:re.Sp. 55-60 - 816:li.Sp. 1-5.54-59 |
|---|---|
| Another potential candidate for a synaptic tag that has recently received significant attention is the actin microfilament network at the synapse. The actin network in neurons is extremely dynamic, and these dynamics have been shown to change with activity. Studies have shown that ubiquitin-mediated proteolysis of the regulatory subunit of PKA results in a persistently active kinase, and that this degradation involves the transcriptional induction of an ubiquitin carboxy-terminal. Together, these findings raise the possibility that local activation of PKA and local regulation of the ubiquitin-proteasome pathway can serve as synaptic tags that combine with transcriptional events (for example, the induction of the ubiquitin carboxy-terminal hydrolase) to produce persistent increase in synaptic strength due to local protein synthesis (Hegde, 2004).
69. Hegde AN (2004) Ubiquitin-proteasome-mediated local protein degradation and synaptic plasticity. Prog Neurobiol 73: 311-357. |
[Seite 815]
Previous studies have shown that UBIQUITIN-mediated proteolysis of the regulatory subunit of PKA results in a persistently active kinase13, and that this degradation involves the transcriptional induction of a ubiquitin carboxy-terminal hydrolase14,15. Together [Seite 816] PKA and local regulation of the ubiquitin–PROTEASOME pathway can serve as synaptic tags that combine with transcriptional events (for example, the induction of the ubiquitin carboxy-terminal hydrolase) to produce persistent and local synaptic strengthening. [...] Another potential candidate for a synaptic tag that has recently received significant attention is the actin microfilament network at the synapse. The actin network in neurons is extremely dynamic, and these dynamics have been shown to change with activity27,28. 14. Hegde, A. N. et al. Ubiquitin C-terminal hydrolase is an immediate–early gene essential for long-term facilitation in Aplysia. Cell 89, 115–126 (1997). 15. Chain, D. G. et al. Mechanisms for generating the autonomous cAMP-dependent protein kinase required for long-term facilitation in Aplysia. Neuron 22, 147–156 (1999). 27. Fischer, M., Kaech, S., Wagner, U., Brinkhaus, H. & Matus, A. Glutamate receptors regulate actin-based plasticity in dendritic spines. Nature Neurosci. 3, 887–894 (2000). 28. Star, E. N., Kwiatkowski, D. J. & Murthy, V. N. Rapid turnover of actin in dendritic spines and its regulation by activity. Nature Neurosci. 5, 239–246 (2002). |
Ohne Hinweis auf eine Übernahme. |
|
| [14.] Sng/Fragment 038 15 - Diskussion Bearbeitet: 22. May 2016, 21:50 Schumann Erstellt: 5. January 2014, 16:26 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 38, Zeilen: 15-20 |
Quelle: Sajikumar 2005 Seite(n): 5, Zeilen: 1-8 |
|---|---|
| Thus heterosynaptic induction of either LTD/LTP on two sets of independent synaptic inputs S1 and S2 can lead to late-associative interactions: early-LTD in S2 was transformed into a late-LTD, if late-LTP was induced in S1 (Fig. 3). The synthesis of process-independent PRPs by late-LTP in S1 was sufficient to transform early- into late-LTD in S2 when process-specific synaptic tags were set. | [My studies show that in rat hippocampal slices in vitro, the induction of protein synthesis-dependent late-LTD is also] characterized by processes of ´synaptic tagging´ and that heterosynaptic induction of either LTD or LTP on two sets of independent synaptic inputs S1 and S2 can lead to late-associative interactions between LTD- and LTP-inputs: early-LTD in a synaptic input S2 was transformed into a late-LTD, if late-LTP was induced in a synaptic input S1 of the same neuronal population within a distinct time interval. The synthesis of process-independent PRPs by late-LTP in S1 was sufficient to transform early- into late-LTD in S2 when process-specific synaptic tags were set. |
Ohne jeden Hinweis auf eine Übernahme. |
|
| [15.] Sng/Fragment 042 01 - Diskussion Bearbeitet: 22. May 2016, 21:54 Schumann Erstellt: 5. January 2014, 16:36 (Graf Isolan) | Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng, Verschleierung |
|
|
|
| Untersuchte Arbeit: Seite: 42, Zeilen: 1-10, 12-21 |
Quelle: Sajikumar 2005 Seite(n): 40, Zeilen: 1-19 |
|---|---|
| 2. Materials and methods
2.1. Hippocampal slice preparation All experiments were performed in right hippocampal slices (400 μm thick) prepared from 7 weeks old male Wistar rats (total number of animals: 310). The animal was stunned by a blow behind the foramen magnum and decapitated (cervical dislocation). Following decapitation, the skin and fur covering the skull were cut away and an incision was made on both sides. The bone covering the brain was prised away and dura removed before transferring the brain into chilled and carbogenated (carbogen: gas consisting of 95% O2 and 5% CO2) artificial cerebrospinal fluid (ACSF) (about 4°C) (Reymann et al., 1985). [...] Divide the remaining part of the brain in the central sulcus by a deep cut using a scalpel and the hippocampal commissure was cut and the right hippocampus was taken out on to the stage of manuel tissue chopper (Cambden, UK), and 400 μm thick slices were cut at 70° transverse to the long axis from the middle third of the right hippocampus. After sectioning, the slices were picked up by a wet artist’s brush, floated in a petri dish containing the cooled and carbogenated ACSF, and immediately transferred to the nylon net in the experimental chamber maintained at 32°C by a wide bored pipette. One of the critical points which elapse between the removal of the brain and the placing of the slices in the chamber is that slice preparation should be performed in less than 3 min [and favourably at a temperature of 4°C to minimize cellular metabolism and to avoid irreversible intracellular phase changes.] 133. Reymann KG, Malisch R, Schulzeck K, Brodemann R, Ott T, Matthies H (1985) The duration of long-term potentiation in the CA1 region of the hippocampal slice preparation. Brain Res Bull 15: 249-255. |
2.0. Materials and methods
2.1. Brain slice preparation and incubation All experiments were performed in right hippocampal slices (400 μm thick) prepared from 7 weeks old male Wistar rats (total number of animals: 275). The animal was stunned by a blow behind the foramen magnum and decapitated immediately. Following decapitation, the skin and fur covering the skull were cut away and an incision was made on both sides. The bone covering the brain was prised away and dura removed before transfering the brain into cooled and carbogenated (carbogen: gas consisiting [sic!] of 95% O2 and 5% CO2) artifical cerebro spinal fluid (ACSF) (about 4°C). Cold solution was used to slow down the metabolism of the tissue, to limit the extent of excitotoxic and other kinds of damage occurring during the preparation of slices (Reymann et al., 1985). The hemispheres were separated mid-sagitally by a deep cut using a scalpel and the hippocampal commissure was cut and the right hippocampus was taken out on to the stage of McIIwain tissue chopper (Cambden,UK), and 400 μm slices were cut at 70° transverse to the long axis from the middle third of the right hippocampus. After sectioning, the slices were picked up by a wet artist’s brush, floated in a petri dish containing the cooled and carbogenated ACSF, and immediately transfered to the nylon net in the experimental chamber by a wide bored pipette. One of the critical points which elapses between the removal of the brain and the placing of the slices in the chamber, is that time should not exceed 4 min. Reymann KG, Malisch R, Schulzeck K, Brodemann R, Ott T, Matthies H (1985) The duration of long-term potentiation in the CA1 region of the hippocampal slice preparation. Brain Res Bull 15: 249-255. |
Im Wortlaut übereinstimmend. Ohne Hinweis auf eine Übernahme. |
|
| [16.] Sng/Fragment 043 10 - Diskussion Bearbeitet: 22. May 2016, 21:56 Schumann Erstellt: 5. January 2014, 17:25 (Graf Isolan) | BauernOpfer, Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 43, Zeilen: 10-20 |
Quelle: Sajikumar 2005 Seite(n): 40-41, 42, Zeilen: 40:24-25 - 41:1-6; 42:10-13 |
|---|---|
| When slices are taken out with proper care the responses, observed on stimulation are similar to those seen in intact animals. Slices were incubated within an interface chamber (Fig. 4) at 32°C (carbogenated incubation medium contained 124 mM NaCl, 4.9 mM KCl, 1.2 mM KH2PO4, 2.0 mM MgSO4, 2.0 mM CaCl2, 24.6mM NaHCO3, 10 mM D-glucose). Supply of oxygen was achieved by controlling the gas flow over the surface of the slice (carbogen flow rate: 32 l/h) thus preventing the drying out of the slices (Sajikumar et al., 2005a).
Slices were preincubated for at least 4 h, a quite unusual long period, but it has been shown by the following reasons to be critical for a stable long-term recording as well as the study of late plasticity for up to 16 h, under conditions which resemble the functionality of studies in vivo. 139. Sajikumar S, Navakkode S, Frey JU (2005a) Protein synthesis-dependent long-term functional plasticity: methods and techniques. Curr Opin Neurobiol .. |
[Seite 40]
When slices are taken out with proper care the responses, observed on stimulation are similar [Seite 41] to those seen in intact animals. Slices were incubated within an interface chamber at 32°C (carbogenated incubation medium contained 124 mM NaCl, 4.9 mM KCl, 1.2 mM KH2PO4, 2.0 mM MgSO4, 2.0 mM CaCl2, 24.6mM NaHCO3, 10 mM D-glucose). Supply of oxygen was achieved by controlling the gas flow over the surface of the slice (carbogen flow rate: 18 l/h) thus preventing the drying out of the slices (see Fig. 3). [Seite 42] Slices were preincubated for at least 4 h, a quite unusual long period, but it has been shown by the following reasons to be critical for a stable long-term recording as well as the study of late plasticity for up to 16 h, under conditions which resemble the functionality of studies in vivo. |
Art und Umfang der Übernahme bleiben ungekennzeichnet. Die Nennung eines Artikels, welcher auf der Arbeit Sajikumar (2005) basiert, führt zur Einstufung als "BauernOpfer". |
|
| [17.] Sng/Fragment 044 01 - Diskussion Bearbeitet: 22. May 2016, 21:57 Schumann Erstellt: 5. January 2014, 17:33 (Graf Isolan) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 44, Zeilen: 1-4 |
Quelle: Sajikumar 2005 Seite(n): (41), 43, Zeilen: 43:3-7 |
|---|---|
| [Fig. 4. Interface chamber and electrical set-up for long term extra cellular recording.
(A) An overview of recording chamber and its electrical set-up. (B) Interface chamber with manipulators. (C) Microscopic view of a hippocampal slice located with electrodes.] Hippocampal slices in vitro are characterized by a very low spontaneous activity which may result from an almost ‘absolute rest’ during preincubation. Biochemical studies have shown that metabolic stability is reached in slices after 2-4 h, i.e., metabolite levels require 2-4 h to stabilize, and these levels are then maintained for at [least 8 h of incubation (Whittingham et al., 1984).] 169. Whittingham TS, Lust WD, Christakis DA, Passonneau JV (1984) Metabolic stability of hippocampal slice preparations during prolonged incubation. J Neurochem 43: 689-696. |
[Seite 41]
[Figure 3. Interface chamber and electrical set-up for long term extra cellular recording. (A) An overview of recording chamber and its electrical set-up. (B) Interface chamber with manipulators. (C) Microscopic view of a hippocampal slice located with electrodes.] [Seite 43] Hippocampal slices in vitro are characterized by a very low spontaneous activity which may result from an almost ‘absolute rest’ during preincubation. Biochemical studies have shown that metabolic stability is reached in slices after 2-4 h, i.e., metabolite levels require 2-4 h to stabilize, and these levels are then maintained for at least 8 h of incubation (Whittingham et al., 1984). Whittingham TS, Lust WD, Christakis DA, Passonneau JV (1984) Metabolic stability of hippocampal slice preparations during prolonged incubation. J Neurochem 43: 689-696. |
Bilder und Legende von "Fig. 4" stimmen mit "Figure 3" in Sajikumar (2005) überein. Auch für den übrigen Inhalt von Seite 44 erfolgt kein Hinweis auf eine Übernahme. |
|
| [18.] Sng/Fragment 045 01 - Diskussion Bearbeitet: 9. May 2016, 20:12 WiseWoman Erstellt: 2. January 2014, 18:36 (SleepyHollow02) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 45, Zeilen: 1 ff. (komplett) |
Quelle: Sajikumar 2005 Seite(n): 43-44, Zeilen: 43:5-25 - 44:1-10 |
|---|---|
| [Biochemical studies have shown that metabolic stability is reached in slices after 2-4 h, i.e., metabolite levels require 2-4 h to stabilize, and these levels are then maintained for at] least 8 h of incubation (Whittingham et al., 1984). This includes parameters for the activity of enzymes, second messengers, pH, and others. Interestingly, the value for bio-active molecules which stabilizes at a very low level, if strong electrical stimulation was not delivered to the tissue. We suppose that in addition to processes of the acute slice preparation, low electrical activity may result in the delayed but prolonged metabolic stability at a low level after about 4 h if no stimulation is applied to the tissue. This may lead to a reduction of PRPs to an amount near zero if the half life of the proteins is considered with about 2 h. Thus, starting with functional experiments after a preincubation time of 4-5 h may rectify all slices and neurons to a low but very comparable basal metabolic and plasticity level. Tetanization for instance, would then activate a machinery of processes ‘from zero’ (a situation never occurring in behaving animals) which is mechanistically more useful to determine time constants during plastic events, than it would be the case by using freely behaving untreated rats. If in intact rats protein synthesis is blocked by a pharmacological reversible inhibitor a similar situation as in slices can be created revealing similar time constants for early-LTP in vitro. Unfortunately, currently available reversible protein synthesis inhibitors reduce the synthesis of macromolecules in the intact animal for several hours, making this preparation probably unusable to directly study processes of synaptic tagging with the methods used so far. Thus, slice preparations represent an ideal, however also partially artificial model to determine properties of tagging and late-associativity. Although, most of the problems concerning brain slice incubation are known for a long time, most laboratories start their ‘physiological’ slice experiments after a very short preincubation period of even less than 1 h. Knowing the metabolic instability during that period we prolonged the preincubation of hippocampal slices to at least 4 h to obtain comparable [and more physiological results in describing functional processes in slice preparations.] | [Seite 43]
Biochemical studies have shown that metabolic stability is reached in slices after 2-4 h, i.e., metabolite levels require 2-4 h to stabilize, and these levels are then maintained for at least 8 h of incubation (Whittingham et al., 1984). This includes parameters for the activity of enzymes, second messengers, pH, and others. Interestingly, the value for bio-active molecules which stabilizes then at a very low level, if strong electrical stimulation was not delivered to the tissue. We suppose that in addition to processes of the acute slice preparation, low electrical activity may result in the delayed but prolonged metabolic stability at a low level after about 4 h if no stimulation is applied to the tissue. This may lead to a reduction of PRPs to an amount near zero if the half life of the proteins is considered with about 2 h. Thus, starting with functional experiments after a preincubation time of 4-5 h, may rectify all slices and neurons to a low but very comparable basal metabolic and plasticity level. Tetanization for instance, would then activate a machinery of processes ‘from zero’ (a situation never occurring in behaving animals) which is mechanistically more useful to determine time constants during plastic events, than it would be the case by using freely behaving untreated rats. If in intact rats protein synthesis is blocked by a pharmacological reversible inhibitor a similar situation as in slices can be created revealing similar time constants for early-LTP in vitro. Unfortunately, currently available reversible protein synthesis inhibitors reduce the synthesis of macromolecules in the [Seite 44] intact animal for several hours, making this preparation probably unusable to directly study processes of synaptic tagging with the methods used so far. Thus, slice preparations represent an ideal, however also partially artificial model to determine properties of tagging and late-associativity. Although, most of the problems concerning brain slice incubation are known for a long time, most laboratories start their ‘physiological’ slice experiments after a very short preincubation period of even less than 1 h. Knowing the metabolic instability during that period we prolonged the preincubation of hippocampal slices to at least 4 h to obtain comparable and more physiological results in describing functional processes in slice preparations. |
Weiter unten, auf der Folgeseite, findet sich zwar ein Hinweis auf Sajikumar and Frey, 2004a, nicht aber auf die hier tatsächlich verwendete Quelle. |
|
| [19.] Sng/Fragment 046 01 - Diskussion Bearbeitet: 22. May 2016, 21:37 Schumann Erstellt: 2. January 2014, 18:47 (SleepyHollow02) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 46, Zeilen: 1-21 |
Quelle: Sajikumar 2005 Seite(n): 44-45, Zeilen: 44:7-25, 45:1-9 |
|---|---|
| [Knowing the metabolic instability during that period we prolonged the preincubation of hippocampal slices to at least 4 h to obtain comparable] and more physiological results in describing functional processes in slice preparations. This requirement is supported by additional data such as measuring basal endogenous protein phosphorylation patterns and the translocation of different protein kinase C isoenzymes (α, β and γ) to the membrane as markers of their activation in tissue obtained from hippocampal slices in vitro or from intact, untreated rats. Studies revealed that only slices incubated in the same way as described here showed comparable patterns of phosphorylation and enzyme translocation as detected in the intact animal (Angenstein and Staak, 1997). Although one could argue that specific modifications of slice preparation may circumvent distinct problems raised above, to maintain the complex slice physiology at a level which allows reliable studies of functional plasticity favours a more simple method: to wait (Sajikumar and Frey, 2004a).
Following the preincubation period, the test stimulation strength was determined for each input to elicit a population spike of about 40 % (for LTD studies) or 25 % (for studies conducted to investigate LTP) of its maximal amplitude determined by slice specific input-output relationship. For stimulation, biphasic constant current pulses were used. The baseline was recorded for at least 60 min before LTP/LTD induction. Four 0.2 Hz biphasic, constant-current pulses (0.1 ms per polarity) were used for testing 1, 3, 5, 11, 15, 21, 25, 30 min post-tetanus or 21, 25, 30 min post-LFS and thereafter once every 15 min up to 8 h. Since the two recorded parameters showed either similar time course in the experiments (if the population spike was not abolished after induction of LTD at all), for clarity only the fEPSP data are shown. A detailed description of the experimental protocol for the preparation, incubation and investigation of reliable rat hippocampal CA1 late-LTP/LTD is shown in Fig. 5 (Sajikumar et al., 2005a). 13. Angenstein F, Staak S (1997) Receptor-mediated activation of protein kinase C in hippocampal long-term potentiation: facts, problems and implications. Prog Neuropsychopharmacol Biol Psychiatry 21: 427-454. 137. Sajikumar S, Frey JU (2004a) Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD. Neurobiol Learn Mem 82: 12-25. 139. Sajikumar S, Navakkode S, Frey JU (2005a) Protein synthesis-dependent long-term functional plasticity: methods and techniques. Curr Opin Neurobiol .. |
[Seite 44]
Knowing the metabolic instability during that period we prolonged the preincubation of hippocampal slices to at least 4 h to obtain comparable and more physiological results in describing functional processes in slice preparations. This requirement is supported by additional data such as measuring basal endogenous protein phosphorylation patterns and the translocation of different protein kinase C isoenzymes (α, β and γ) to the membrane as markers of their activation in tissue obtained from hippocampal slices in vitro or from intact, untreated rats. Studies revealed that only slices incubated in the same way as described here showed comparable patterns of phosphorylation and enzyme translocation as detected in the intact animal (Angenstein and Staak, 1997). Although one could argue that specific modifications of slice preparation may circumvent distinct problems raised above, to maintain the complex slice physiology at a level which allows reliable studies of functional plasticity favors a more simple method: to wait (Sajikumar and Frey, 2004a). Following the preincubation period, the test stimulation strength was determined for each input to elicit a population spike of about 40 % (for LTD studies) or 25 % (for studies conducted to investigate LTP and the effect of dopamine application) of its maximal amplitude determined by slice specific [Seite 45] input-output relationship. For stimulation, biphasic constant current pulses were used. The baseline was recorded for at least 60 min before LTP/LTD induction. In the dopamine studies the baseline was recorded for at least 30 min. Four 0.2 Hz biphasic, constant-current pulses (0.1 ms per polarity) were used for testing 1, 3, 5, 11, 15, 21, 25, 30 min post-tetanus or 21, 25, 30 min post-LFS and thereafter once every 15 min up to 8 h (30 min in dopamine series). Since the two recorded parameters showed either similar time course in the experiments (if the population spike was not abolished after induction of LTD at all), for clarity only the fEPSP data are shown. Angenstein F, Staak S (1997) Receptor-mediated activation of protein kinase C in hippocampal long-term potentiation: facts, problems and implications. Prog Neuropsychopharmacol Biol Psychiatry 21: 427-454. Sajikumar S, Frey JU (2004a) Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD. Neurobiol Learn Mem 82: 12-25. |
Der letzte Satz auf der Seite könnte selbst formuliert sein. |
|
| [20.] Sng/Fragment 049 01 - Diskussion Bearbeitet: 22. May 2016, 21:39 Schumann Erstellt: 2. January 2014, 20:25 (SleepyHollow02) | Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Sng |
|
|
|
| Untersuchte Arbeit: Seite: 49, Zeilen: 1-20 (komplett) |
Quelle: Sajikumar 2005 Seite(n): 45-46, Zeilen: 45:11-24 - 46:1-10 |
|---|---|
| [It is also certified that formal approval to conduct the experiments described has been obtained from the animal subjects review board of the institution/local government which can be provided upon] request. All efforts were made to minimize the number of animals used and their suffering.
2.3. Stimulation Protocols: Induction of late-LTD, early-LTD, late-LTP and early-LTP For inducing late-LTD, a strong low-frequency stimulation protocol (SLFS) which consisted of 900 bursts (one burst consisted of 3 biphasic, constant current stimuli at a frequency of 20 Hz, interburst interval: 1 s, i.e. f=1 Hz, stimulus duration 0.2 ms per half-wave; a total number of stimuli of 2700) was found to be the most effective protocol (Sajikumar and Frey, 2003;Sajikumar and Frey, 2004a). This stimulation pattern produced a stable LTD in vitro for at least 8 h. For inducing a transient early-LTD a weak low-frequency stimulation protocol (WLFS) consisting of 900 pulses (f=1 Hz, impulse duration 0.2 ms per half-wave, a total number of stimuli of 900, as ever: biphasic, constant current stimuli) was determined to be the most efficient in inducing early-LTD (Sajikumar and Frey, 2003;Sajikumar and Frey, 2004a). Late-LTP was induced using three stimulus trains of 100 pulses (‘strong’ tetanus: f=100 Hz, stimulus duration 0.2 ms per polarity with 10 min intertrain-intervals) (Frey and Morris, 1997;Frey and Morris, 1998b). In experiments with induction of early-LTP, a single tetanus with 21 pulses was used (`weak’ tetanus: f=100 Hz, stimulus duration 0.2 ms per polarity, population spike threshold stimulus intensity for tetanization (Frey and Morris, 1997;Frey and Morris, 1998b). 57. Frey U, Morris RG (1997) Synaptic tagging and long-term potentiation. Nature 385: 533-536. 59. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. 136. Sajikumar S, Frey JU (2003) Anisomycin inhibits the late maintenance of long-term depression in rat hippocampal slices in vitro. Neurosci Lett 338: 147-150. 137. Sajikumar S, Frey JU (2004a) Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD. Neurobiol Learn Mem 82: 12-25. |
[Seite 45]
It is also certified that formal approval to conduct the experiments described has been obtained from the animal subjects review board of our institution/local government which can be provided upon request. All efforts were made to minimize the number of animals used and their suffering. 2.2. Stimulation Protocols: Inuction [sic] of late-LTD, early-LTD, late-LTP, early-LTP and depotentiaton For inducing late-LTD, a strong low-frequency stimulation protocol (SLFS) which consisted of 900 bursts (one burst consisted of 3 stimuli at a frequency of 20 Hz, interburst interval=1 s, i.e. f=1 Hz, stimulus duration 0.2 ms per half-wave; a total number of stimuli of 2700) was found to be the most effective protocol (Sajikumar and Frey, 2003;Sajikumar and Frey, 2004a). This stimulation pattern produced a stable LTD in vitro for at least 8 h. For inducing a transient early-LTD a weak low-frequency stimulation protocol [Seite 46] (WLFS) consisting of 900 pulses (f=1 Hz, impulse duration 0.2 ms per half-wave, a total number of stimuli of 900) was determined to be the most efficient in inducing early-LTD (Sajikumar and Frey, 2003;Sajikumar and Frey, 2004a). Late-LTP was induced using three stimulus trains of 100 pulses (‘strong’ tetanus: f=100 Hz, stimulus duration 0.2 ms per polarity with 10 min intertrain-intervals) (Frey and Morris, 1997;Frey and Morris, 1998b). In experiments with induction of early-LTP, a single tetanus with 21 pulses was used (`weak’ tetanus: f=100 Hz, stimulus duration 0.2 ms per polarity, population spike threshold stimulus intensity for tetanization) (Frey and Morris, 1997;Frey and Morris, 1998b). Frey U, Morris RG (1997) Synaptic tagging and long-term potentiation. Nature 385: 533-536. Frey U, Morris RG (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts of late-LTP. Neuropharmacology 37: 545-552. Sajikumar S, Frey JU (2003) Anisomycin inhibits the late maintenance of long-term depression in rat hippocampal slices in vitro. Neurosci Lett 338: 147-150. Sajikumar S, Frey JU (2004a) Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD. Neurobiol Learn Mem 82: 12-25. |
Nur auf Sajikumar and Frey, 2003 bzw. 2004a, wird hingewiesen |
|