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Autor     Sreedharan Sajikumar
Titel    Functional plasticity in the hippocampal slices in vitro
Jahr    2005
Umfang    117 S.
Anmerkung    Magdeburg, Univ., Diss., 2005
URL    http://diglib.uni-magdeburg.de/Dissertationen/2005/sresajikumar.pdf

Literaturverz.   

nein
Fußnoten    nein
Fragmente    16


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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.


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.


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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan)

[2.] Sng/Fragment 002 01 - Diskussion
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Acknowledgements

It is a pleasure to thank those who gave their support in different ways to complete this work and I would like to convey my heartfelt gratitude and sincere appreciation. First and foremost I would like to express my sincere thanks to my supervisor, Prof. Dr. Julietta Uta Frey, for the guidance and support that she provided throughout the course of this work. Moreover her encouragement, helpfulness and moral support helped me, not only to overcome but also to persevere and excel, which has increased my confidence and abilities as a researcher.

I am especially grateful to Dr. Sreedharan Sajikumar for all kinds of encouragement and support which helped me to progress every time.

I am highly indebted to Manuela Homeyer, who made everything easier for me by her timely help, and co-operation during the entire period of this work.

I express my sincere thanks to Dr. Volker Korz for all his help and scientific discussions.

I wish to acknowledge the help and valuable suggestions given to me by Dr. Thomas Behnisch, Dr. Sabine Frey, Dr. Anna Karpova, Dr. Tariq Ahmed and Dr. Hadir Hassan. I would like to thank Dr. Anoopkumar Thekkuveettil, Dept. of Molecular Medicine, SCTIMST, Thiruvananthapuram, Kerala, India, for guiding me into the field of Neuroscience. I express my sincere thanks to Diana Koch, Gusalija Behnicsh, Silvia Vieweg, Sybille Tschorn, Sabina Opitz, Diana Marenda, Jeanette Maiwald and Jürgen Buggert for their excellent technical assistance and co-operation during the course of this study. I would like to thank my colleagues Dasha, Marina, Sergey, Schukrat, Frank and all my friends who cooperated with me during the period of this work.

And last, but most of all, to my parents, and sisters, I owe everything; they sustain me in all that I do and it is to them that this work is dedicated with love. Finally, my best thanks of all goes to God, who has always been there for me.

Sincerely [...]

ACKNOWLEDGEMENTS

I feel extremely fortunate to have the privilege of working under the inspiring supervision of Prof. Dr. Julietta Uta Frey. I sincerely thank her for the constant support, encouragement and constructive criticisms. Her unstinted guidance and monitoring of this work has enabled me to take the right direction.

I am highly grateful to Sabine Opitz for her excellent technical assistance during the initial period of this work.

I am highly indebted to Manuela Homeyer for her timely help, and co-operation extended to me during the entire period of this work.

I wish to acknowledge the help and valuable suggestions given to me by Dr. Maxim Sokolov, Dr. Volker Korz, Dr. Sabine Frey, Dr. Thomas Behnisch, Dr. Tariq Ahmed and Dr. Anna Karpova.

I express my sincere thanks to Gusalija Behnisch, Sybille Tschorn, Diana Koch and Silvia Vieweg for their excellent technical assistance and co-operation during the course of this study.

I am specially thankful to all of my colleagues especially to Sheeja Navakkode for her help and scientific discussions.

The constant support and encouragement extended to me by Prof. Dr. T. Ramakrishna and Prof. Dr. V. K. Sasidharan is acknowledged here with great fondness and sincerity. Above all I wish to express my deep sense of gratitude and special indebtedness to my parents, brothers and sister for their love, tolerance and moral support, which made me possible to stand at this point of life.

S. Sajikumar

Anmerkungen
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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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

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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.
Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

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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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Hebb (1949) wird in Sng nicht aufgeschlüsselt.

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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.

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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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

"Figure 2" ist ebenfalls identisch.

Sichter
(Graf Isolan) Schumann

[8.] Sng/Fragment 034 15 - Diskussion
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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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sng hat einfach die Reihenfolge der Absätze umgestellt; ansonsten erfolgt bis auf Auslassungen kein inhaltlicher Eingriff.

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(Graf Isolan) Schumann

[9.] Sng/Fragment 035 01 - Diskussion
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[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.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

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(Graf Isolan) Schumann

[10.] Sng/Fragment 038 15 - Diskussion
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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.
Anmerkungen

Ohne jeden Hinweis auf eine Übernahme.

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(Graf Isolan) Schumann

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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.

Anmerkungen

Im Wortlaut übereinstimmend. Ohne Hinweis auf eine Übernahme.

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(Graf Isolan) Agrippina1

[12.] Sng/Fragment 043 10 - Diskussion
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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.

Anmerkungen

Art und Umfang der Übernahme bleiben ungekennzeichnet. Die Nennung eines Artikels, welcher auf der Arbeit Sajikumar (2005) basiert, führt zur Einstufung als "BauernOpfer".

Sichter
(Graf Isolan) Schumann

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[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.

Anmerkungen

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.

Sichter
(Graf Isolan) Schumann

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[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.

Anmerkungen

Weiter unten, auf der Folgeseite, findet sich zwar ein Hinweis auf Sajikumar and Frey, 2004a, nicht aber auf die hier tatsächlich verwendete Quelle.

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[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.

Anmerkungen

Der letzte Satz auf der Seite könnte selbst formuliert sein.

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(SleepyHollow02) Schumann

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[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.

Anmerkungen

Nur auf Sajikumar and Frey, 2003 bzw. 2004a, wird hingewiesen

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