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23 gesichtete, geschützte Fragmente: Plagiat

[1.] Br/Fragment 008 03 - Diskussion
Bearbeitet: 21. May 2016, 18:01 Schumann
Erstellt: 31. December 2013, 15:47 (Graf Isolan)
Benfenati 2007, Br, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Quelle: Benfenati 2007
Seite(n): 59, Zeilen: re.Sp. 3-7, (7-13), 13-18
The most distinctive feature of the mammalian central nervous system is its ability to adapt to the environment and to improve its performance over time and experience. [An important basis for this peculiar property is the plastic nature of the synapses, i.e. the capacity to change their signaling strength, both in short and long term, in response to specific patterns of synaptic activity.] The neural changes evoked by the stimuli can persist even for very long times, virtually for the whole life of the individual. This neural plasticity represents the basis of higher brain functions such as learning and memory. Synaptic plasticity and the cellular bases of memory

The major and most distinctive feature of the nervous system is the astonishing ability to adapt to the environment and to improve its performance over time and experience. [This peculiar property, collectively named “plasticity”, has been precisely defined at the end of the XIX century by Santiago Ramon y Cajal as “the property by virtue of which sustained functional changes occur in particular neuronal systems following the administration of appropriate environmental stimuli or the combination of different stimuli”.] Since the neural changes evoked by the stimuli can persist for very long times, virtually for the whole life of the individual, it seems clear that neural plasticity represents the basis of the higher brain functions such as learning and memory [or, conversely, that the built-in property of neural plasticity allows experience to shape both functionally and structurally the nervous system].

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Das von Benfenati eingeschobene Zitat wurde paraphrasiert und geht daher nicht in die Zeilenzählung ein.

Sichter
(Graf Isolan) Schumann

[2.] Br/Fragment 008 15 - Diskussion
Bearbeitet: 21. May 2016, 18:02 Schumann
Erstellt: 31. December 2013, 16:06 (Graf Isolan)
Benfenati 2007, Br, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 8, Zeilen: 15-25
Quelle: Benfenati 2007
Seite(n): 60, 61, 62, Zeilen: 60:re.Sp. 10-13.16-20; 61:li.Sp. 1ff. - re.Sp. 1-2; 62:li.Sp. 13-17
Implicit memory refers to information storage to perform various reflexive or perceptual tasks and is recalled unconsciously. The implicit memory is more robust and may last for all our life even in the absence of further practice (Squire, 2004). Implicit memory involves a heterogeneous collection of memory functions and types of learned behaviors such as reflexive conditioning, fear conditioning and priming. The explicit memory is concerned with the factual knowledge of persons, things, notions and is recalled by a deliberate and conscious effort.

Explicit memory can be further classified as episodic and semantic memory. Episodic memory allows us to remember personal events and experience, on the other hand semantic memory is a sort of public memory for facts and notions.


Squire LR (2004) Memory systems of the brain: a brief history and current perspective. Neurobiol Learn Mem 82:171-177.

[Seite 60]

The first one refers to information storage to perform various reflexive or perceptual tasks is also referred to as non-declarative or implicit memory because it is recalled unconsciously. [...] Implicit memory is a heterogeneous collection of memory functions and types of learned behaviours such as reflexive learning (sensitization, habituation), classical conditioning, fear conditioning, procedural memory (for skills and habits) and priming [(the recall of words or objects from a previous unconscious exposure to them).]

[Seite 61]

The second form of memory, called declarative or explicit memory because it is recalled by a deliberate and conscious effort, concerns factual knowledge of persons, things, notions and places. Declarative memory can be further classified as episodic or autobiographic memory and semantic memory. Episodic memory allows us to remember personal events and experience and, being a link between what we are and what we have been, gives us the sense of our individuality. On the other hand, semantic memory is a sort of public memory for facts and notions[, be they general or autobiographical (Fig. 4).]

[Seite 62]

However, while explicit memory fades relatively rapidly in the absence of recall and refreshing, implicit memory is much more robust and may last for all our life even in the absence of further practice (4, 5).


4. Blackemore C. Mechanics of the mind. Cambridge; Cambridge University Press, 1977.

5. Kandel ER, Pittenger C. The past, the future and the biology of memory storage. Philos Trans R Soc Lond B Biol Sci 1999; 354: 2027-52.

Anmerkungen

Zwar zusammengeschnitten, doch bleibt das Original unverkennbar. Dennoch ohne jeden Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[3.] Br/Fragment 009 01 - Diskussion
Bearbeitet: 21. May 2016, 18:07 Schumann
Erstellt: 4. January 2014, 20:07 (Graf Isolan)
Benfenati 2007, Br, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Verschleierung

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[The] explicit memory fades relatively rapidly in the absence of recall and refreshing and prone to distortion (Cohen and Squire, 1980; Squire., et al., 1993; Squire, 2004).

Neuropsychological studies on patients, mainly pioneered by Brenda Millner with the famous H.M. case, have shown that the multiple memory systems involve distinct brain areas, especially the medial temporal lobe, and exhibit distinctive features (Scoville and Milner, 1957).


• Cohen NJ, Squire LR (1980) Preserved learnign and retention of pattern analysing skill in amnesia: dissociation of knowing how and knowing that. Science.210:207-10.

• Scoville WB and Milner B (1957) Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psychiatry.20:11-21.

• Squire LR (1993) The hippocampus and spatial memory. Trends Neurosci 16:56-7.

• Squire LR (2004) Memory systems of the brain: a brief history and current perspective. Neurobiol Learn Mem 82:171-177.

[Seite 61]

Neuropsychological studies on neurological patients, mainly pioneered by Brenda Millner with the famous H.M. case, have shown that the multiple me-

[Seite 62]

mory systems involve distinct brain areas and exhibit distinctive features. Thus, explicit memory needs an intact medial temporal lobe (hippocampus), [...]

However, while explicit memory fades relatively rapidly in the absence of recall and refreshing, implicit memory is much more robust and may last for all our life even in the absence of further practice (4, 5).


4. Blackemore C. Mechanics of the mind. Cambridge; Cambridge University Press, 1977.

5. Kandel ER, Pittenger C. The past, the future and the biology of memory storage. Philos Trans R Soc Lond B Biol Sci 1999; 354: 2027-52.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[4.] Br/Fragment 009 09 - Diskussion
Bearbeitet: 21. May 2016, 18:04 Schumann
Erstellt: 1. January 2014, 15:51 (Graf Isolan)
Br, Fragment, Gesichtet, Maren und Baudry 1995, SMWFragment, Schutzlevel sysop, Verschleierung

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Quelle: Maren und Baudry 1995
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In 1949 Donald Hebb in his book “The Organization of Behavior” proposed that memories are stored in the mammalian brain as stronger synaptic connections between neurons active during learning. The specific mechanism he suggested to bring about these changes in synaptic transmission is relatively simple. In his now classic book, “The Organization of Behavior” (1949), Donald Hebb proposed that memories are stored in the mammalian brain as stronger synaptic connections between neurons active during learning. The specific mechanism he suggested to bring about these changes in synaptic transmission is relatively simple.
Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[5.] Br/Fragment 009 19 - Diskussion
Bearbeitet: 21. May 2016, 18:05 Schumann
Erstellt: 1. January 2014, 16:41 (Graf Isolan)
Br, Fragment, Gesichtet, Maren und Baudry 1995, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 9, Zeilen: 19-24
Quelle: Maren und Baudry 1995
Seite(n): 1, Zeilen: li.Sp. 23-27 - re.Sp. 1-3.11-16
In other words, correlation/or association of pre- and post-synaptic activity in two neurons elicits some change in one or both of the neurons such that the synaptic connection between them is strengthened (Hebb, 1949). These kind of modified synapses are referred as “Hebbian synapses” or “Hebb synapses”. Later this became a theoretical foundation for many neurobiological and computational models of “synaptic plasticity” and has revolutionized thinking about the nature of the neural [mechanisms of learning and memory formation.]

• Hebb DO (1949) The Organization of Behavior, Wiley: New York.

[Seite 1]

In other words, correlation (or association) of pre- and post-synaptic activity in two neurons elicits some change in one or both of the neurons such that the synaptic connection between them is strengthened (Hebb, 1949). We will refer to synapses that are modified in this manner as “Hebbian synapses” or “Hebb synapses.” [...] The importance of Hebb’s contribution in this regard cannot be contested: the Hebb synapse is a construct that has become a theoretical foundation for many neurobiological and computational models of synaptic plasticity and has revolutionized thinking about the nature of the neural mechanisms of learning and memory formation.


Hebb, D. O. (1949). The organization of behavior. New York: Wiley.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[6.] Br/Fragment 011 06 - Diskussion
Bearbeitet: 21. May 2016, 17:59 Schumann
Erstellt: 1. January 2014, 11:31 (Graf Isolan)
Br, Fragment, Gesichtet, O’Neal 2007, SMWFragment, Schutzlevel sysop, Verschleierung

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The hippocampus proper is composed of regions with tightly packed pyramidal neurons, mainly as CA1, CA2 and CA3. The CA1-CA3 subfields are called the Cornu Ammonis or Ammon’s horn for its resemblance to a ram’s horn of the Egyptian God Ammon. The CA1 region is also called the superior region, which composed of tightly packed pyramidal cells. These cells become loosely packed in CA2 and CA3 region (also called the inferior region) and this thinning denotes the boundary between the two areas. The CA3 region marks the transition from the hippocampus proper to the dentate gyrus (Isaacson, 1982). The dentate gyrus is part of the large hippocampal formation (which is often referred to simply as the hippocampus) that includes the dentate gyrus and the subiculum (Giap et al., 2000).

• Giap BT, Jong CN, Ricker JH, Cullen NK, Zafonte RD (2000) The hippocampus: anatomy, pathophysiology, and regenerative capacity. J Head Trauma Rehabil.15:875-94.

• Isaacson R (1982) The Limbic System (2nd ed). New York, London. Plenum Press.

The hippocampus proper is divided into four zones called the cornu Ammonis (CA regions 1-4) or Ammon’s horn for its supposed resemblance to a ram’s horn. The CA1 region forms what is also called the superior region, which is comprised of a dense layer of pyramidal cells. These cells become less dense as they approach the CA3 region (also called the inferior region) and this thinning denotes the boundary between the two areas. The CA4 region marks the transition from the hippocampus proper (specifically the CA3) to the dentate gyrus (Isaacson, 1982). The dentate gyrus is part of the larger hippocampal formation (which is often referred to simply as the hippocampus) that encompasses the four CA regions, the dentate gyrus, and the subiculum (Giap et al., 2000).

Isaacson, R., (1982). The Limbic System (2nd ed.). New York, London. Plenum Press.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

O’Neal (2007) enthält keine Aufschlüsselung für (Giap et al., 2000).

Sichter
(Graf Isolan) Schumann

[7.] Br/Fragment 011 18 - Diskussion
Bearbeitet: 21. May 2016, 17:57 Schumann
Erstellt: 31. December 2013, 15:06 (Graf Isolan)
Br, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wilson 2005

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Seite: 11, Zeilen: 18-21
Quelle: Wilson 2005
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The hippocampus receives highly processed multi-modal information from the association cortices (Amaral and Witter, 1995), that is, inputs from all the sensory modalities, vision, hearing, touch, etc, have already converged and been preliminarily associated with one another by the time they reach the hippocampus.

• Amaral DG, Witter MP (1995) Hippocampal formation. In: G. Paxinos, Editor, The Rat Nervous System (2nd edition ed.) Academic Press, San Diego (1995), pp. 443–493.

The hippocampus receives highly processed multi-modal information from the association cortices (Amaral and Witter, 1995). That is, inputs from all the sensory modalities, vision, hearing, touch, etc., have already converged and been preliminarily associated with one another by the time they reach the hippocampus.

Amaral, D.G., and Witter, M.P. (1995). Hippocampal formation. In: The rat nervous system, 2nd ed, Paxinos, G. ed., (San Diego: Academic Press) pp. 443-493.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[8.] Br/Fragment 011 21 - Diskussion
Bearbeitet: 21. May 2016, 17:59 Schumann
Erstellt: 2. January 2014, 22:33 (Graf Isolan)
Br, Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Verschleierung

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Quelle: Sajikumar 2005
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The hippocampus has direct connections to the entorhinal cortex via the subiculum. Outputs from these structures can affect many other areas of the brain. For example the entorhinal cortex projects to the cingulated cortex, which has connections to the temporal lobe cortex, orbital cortex, and olfactory bulb. Thus, all of these areas can be influenced by hippocampal output, primarily from CA1. It has direct connections to the entorhinal cortex (via the subiculum) and the amygdala. Outputs from these structures can then affect many other areas of the brain (Fig. 1). For example, the entorhinal cortex projects to the cingulate cortex, which has a connection to the temporal lobe cortex, orbital cortex, and olfactory bulb. Thus, all of these areas can be influenced by hippocampal output, primarily from CA1.
Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[9.] Br/Fragment 012 01 - Diskussion
Bearbeitet: 21. May 2016, 18:25 Schumann
Erstellt: 2. January 2014, 22:37 (Graf Isolan)
Br, Fragment, Gesichtet, SMWFragment, Sajikumar 2005, Schutzlevel sysop, Verschleierung

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[The entorhinal cortex is a] major source of inputs to the hippocampus collecting information from the cingulated cortex, amygdale, orbital cortex and olfactory bulb (Johnson and Amaral, 1998). The hippocampus receives inputs via the precommissural branch of the fornix from the septal nuclei.

• Johnson D, Amaral D.G (1998) Hippocampus. In: G.M. Shepherd, Editor, The synaptic organization of the brain (4th ed.) Oxford University Press, Oxford. pp. 417–45.

The entorhinal cortex has a major source of inputs to the hippocampus, collecting information from the cingulate cortex, temporal lobe cortex, amygdala, orbital cortex, and olfactory bulb (Amaral and Witter, 1989). The hippocampus receives inputs via the precommissural branch of the fornix from the septal nuclei.

Amaral DG, Witter MP (1989) The three-dimensional organization of the hippocampal formation: a review of anatomical data. Neuroscience 31: 571-591.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[10.] Br/Fragment 012 05 - Diskussion
Bearbeitet: 21. May 2016, 17:55 Schumann
Erstellt: 31. December 2013, 14:53 (Graf Isolan)
Br, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wilson 2005

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Information flow within the hippocampus formation is classically described as a trisynaptic circuit, signifying a cascade of processing (Amaral, 1993; Amaral and Witter, 1995), although there is also evidence of some feedback processing within the hippocampus (Penttonen et al., 1997). The first synaptic connections to enter the hippocampus arise from layer II of the entorhinal cortex, which sends highly processed sensory information through the perforant path to dentate gyrus. These axons also branch off collaterals to the CA3 region. The second synaptic connections come from the dentate gyrus via the mossy fibres to the CA3. Thus the information from the entorhinal cortex arrives to CA3 both monosynaptically and disynaptically. This information is further processed within CA3 through auto-association fibres, which connect the CA3 pyramidal cells with one another. The third connection in the trisynaptic circuit brings the information from the CA3 cells via the Schaffer collaterals to the CA1 cells. Interestingly, CA1 also receives the information from the entorhinal cortex twice, trisynaptically from CA3 and monosynaptically through a direct connection from layer III of the entorhinal cortex (Amaral, 1993; Amaral and Witter, 1995). CA1 projects its processed information to subiculum, where once again the entorhinal cortex has also sent its information. Finally, the information is returned from CA1 to the entorhinal cortex both monosynaptically through direct projections from CA1 and disynaptically through the subiculum. Fig.1 represents the major intrinsic connections of the hippocampal formation. These simultaneous projections appear to be a guiding principle of the hippocampal circuit, allowing the processed information to be compared with a form of the original information at every step [through parallel processing in addition to the classical serial cascade of processing (Amaral, 1993).]

• Amaral DG (1993) Emerging principles of hippocampal organization. Current Opinion in Neurobiology 3:225-229.

• Amaral DG, Witter MP (1995) Hippocampal formation. In: G. Paxinos, Editor, The Rat Nervous System (2nd edition ed.) Academic Press, San Diego (1995), pp. 443–493.

• Penttonen M, Kamondi A, Sik A, Acsády L, Buzsáki G (1997) Feed-forward and feed-back activation of the dentate gyrus in vivo during dentate spikes and sharp wave bursts. Hippocampus 7:437-50.

[Seite 29]

Information flow within the hippocampus formation is classically described as a trisynaptic circuit, signifying a cascade of processing (Amaral, 1993; Amaral and Witter, 1995), although there is also evidence of some feedback processing within the hippocampus (Penttonen et al., 1997).

[Seite 30]

The first synaptic connections to enter the hippocampus arise from layer II of the entorhinal cortex, which sends highly processed sensory information through the perforant path to the dentate gyrus. These axons also branch off collaterals to the CA3 region. The second synaptic connections come from the dentate gyrus via the mossy fibers to the CA3. Thus the information from the entorhinal cortex arrives to CA3 both monosynaptically and disynaptically. This information is further processed within CA3 through auto-association fibers, which connect the CA3 pyramidal cells with one another. The third connection in the trisynaptic circuit brings the information from the CA3 cells via the Schaffer collaterals to the CA1 cells. Interestingly, CA1 also receives the information from the entorhinal cortex twice, trisynaptically from CA3 and monosynaptically through a direct connection from layer III of the entorhinal cortex (Amaral, 1993; Amaral and Witter, 1995).

CA1 projects its processed information to subiculum, where once again the entorhinal cortex (layer III) has also sent its information. Finally, the information is returned from CA1 to the entorhinal cortex (in this case the deep layers IV-VI) both monosynaptically through direct projections from CA1 and disynaptically through the subiculum. These simultaneous projections appear to be a guiding principle of the hippocampal circuit, allowing the processed information to be compared with a form of the original information at every step through parallel processing in addition to the classical serial cascade of processing (Amaral, 1993).


Amaral, D.G. (1993). Emerging principles of intrinsic hippocampal organization. Curr. Opin. Neurobiol. 3: 225-229.

Amaral, D.G., and Witter, M.P. (1995). Hippocampal formation. In: The rat nervous system, 2nd ed, Paxinos, G. ed., (San Diego: Academic Press) pp. 443-493.

Penttonen, M., Kamondi, A., Sik, A., Acsady, L., and Buzsaki, G. (1997). Feed-forward and feed-back activation of the dentate gyrus in vivo during dentate spikes and sharp wave bursts. Hippocampus 7: 437-450.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[11.] Br/Fragment 014 03 - Diskussion
Bearbeitet: 21. May 2016, 17:53 Schumann
Erstellt: 31. December 2013, 14:09 (Graf Isolan)
Br, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Spruston 2008

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The long axon of each pyramidal neuron typically emanates from the base of the soma and branches profusely, making excitatory glutamatergic synaptic contacts along its length. The dendritic tree of a pyramidal neuron has two distinct domains: the basal and apical dendrites, which descend from the base and the apex of the soma, respectively. All pyramidal neurons have several, relatively short basal dendrites. Usually one large apical dendrite connects the soma to a tuft of dendrites. This main apical dendrite bifurcates before giving rise to the tuft at a variable distance from the soma. In some cases the resulting dendrites each bifurcate again. Oblique apical dendrites emanate from the main apical dendrite at various angles.

The distinct morphologies of basal and apical dendrites suggest that inputs to these domains might be integrated differently. Furthermore, different dendritic domain receive distinct synaptic inputs, for instance, CA1 neurons receive input to the distal tuft from the entorhinal cortex through the perforant path and from the thalamus, whereas the remainder of the dendrites receive input from CA3 through the Schaffer collaterals. Furthermore, CA3 neurons that are distant from CA1 project primarily to apical dendrites, whereas CA3 neurons that are closer to CA1 project more heavily to basal dendrites. The functional significance of this arrangement remains mysterious.

[Seite 206]

The lone axon of each pyramidal neuron typically emanates from the base of the soma and branches profusely, making many excitatory glutamatergic synaptic contacts along its length. [...]

The dendritic tree of a pyramidal neuron has two distinct domains: the basal and the apical dendrites, which descend from the base and the apex of the soma, respectively (FIG. 1a). All pyramidal neurons have several relatively short basal dendrites. Usually, one large apical dendrite connects the soma to a tuft of dendrites. This main apical dendrite bifurcates before giving rise to the tuft at a variable distance from the soma. In some cases the resulting ‘twin’ apical dendrites each bifurcate again4–6. Oblique apical dendrites emanate from the main apical dendrite at various angles.

[Seite 208]

The distinct morphologies of basal and apical dendrites suggest that inputs to these domains might be integrated differently. Furthermore, different dendritic domains receive distinct synaptic inputs. For example, CA1 neurons receive input to the distal tuft from the entorhinal cortex through the perforant path and from the thalamus, whereas the remainder of the dendrites receive input from CA3 through the Schaffer collaterals. Furthermore, CA3 neurons that are distant from CA1 project primarily to apical dendrites, whereas CA3 neurons that are closer to CA1 project more heavily to basal dendrites27,28. The functional significance of this arrangement remains mysterious.


4. Bannister, N. J. & Larkman, A. U. Dendritic morphology of CA1 pyramidal neurones from the rat hippocampus: I. Branching patterns. J. Comp. Neurol. 360, 150–160 (1995).

5. Ito, M., Kato, M. & Kawabata, M. Premature bifurcation of the apical dendritic trunk of vibrissaresponding pyramidal neurones of X‑irradiated rat neocortex. J. Physiol. 512, 543–553 (1998).

6. DeFelipe, J. & Farinas, I. The pyramidal neuron of the cerebral cortex: morphological and chemical characteristics of the synaptic inputs. Prog. Neurobiol. 39, 563–607 (1992).

27. Ishizuka, N., Weber, J. & Amaral, D. G. Organization of intrahippocampal projections originating from CA3 pyramidal cells in the rat. J. Comp. Neurol. 295, 580–623 (1990).

28. Li, X. G., Somogyi, P., Ylinen, A. & Buzsaki, G. The hippocampal CA3 network: an in vivo intracellular labeling study. J. Comp. Neurol. 339, 181–208 (1994).

Anmerkungen

Ohne Hinweis auf eine Übernahme.

"long" statt "lone", "instance" statt "example" sind die einzigen "substantiellen" Änderungen, welche Br hier durchführt.

Sichter
(Graf Isolan) Schumann

[12.] Br/Fragment 015 13 - Diskussion
Bearbeitet: 21. May 2016, 18:14 Schumann
Erstellt: 4. January 2014, 21:02 (Graf Isolan)
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(Wong et al., 1979; Benardo et al., 1982; Wong and Stewart, 1992; Andreasen and Lambert, 1995; Kamondi et al., 1998). The restriction of calcium spike initiation to the dendrites is likely the result of strong activation of potassium channels in the soma and proximal dendrites by sodium-dependent action potentials. Calcium spikes appear to detect specific spatial and temporal combinations of synaptic input and signal these events to the synaptic target of neuron through the generation of a distinctive burst of action potential out put [sic] (Lisman, 1997).

Calcium spikes may serve as a powerful regulator of synaptic plasticity, because they would likely mediate a substantial influx of calcium through voltage-gated calcium channels. Furthermore, the prolonged depolarizations mediated by calcium spikes would relieve the voltage-dependent block on NMDA receptors and induce additional calcium influx. Calcium spikes could thus serve as a robust cellular mechanism by which synaptic inputs conveying temporally correlated information [might be selectively reinforced.]


• Andreasen M, Lambert JD (1995) The excitability of CA1 pyramidal cell dendrites is modulated by a local Ca (2+)-dependent K(+)-conductance. Brain Res. 698:193-203.

• Benardo LS, Prince DA (1982) Dopamine modulates a Ca2+-activated potassium conductance in mammalian hippocampal pyramidal cells. Nature 297:76-79.

• Kamondi A, Acsády L, Buzsáki G (1998) Dendritic spikes are enhanced by cooperative network activity in the intact hippocampus. J Neurosci 18:3919-28.

• Lisman, J. (1997) Bursts as a unit of neural information: making unreliable synapses reliable. Trends In Neuroscience 20:38-43.

• Wong RKS, Prince DA, Basbaum AI (1979) Intradendritic recordings from hippocampal neurons. Proc Natl Acad Sci USA 76:986-990.

• Wong RK, Stewart M (1992) Different firing patterns generated in dendrites and somata of CA1 pyramidal neurones in guinea-pig hippocampus. J Physiol 457:675-87.

[Seite 8789]

(Wong et al., 1979; Benardo et al., 1982; Wong and Stewart, 1992; Andreasen and Lambert, 1995; Kamondi et al., 1998).

[...] The restriction of calcium spike initiation to the dendrites is likely the result of strong activation of potassium channels in the soma and proximal dendrites by sodium-dependent action potentials.

[Seite 8797]

Thus, in a variety of brain areas, calcium spikes appear to detect specific spatial and temporal combinations of synaptic input and signal these events to the synaptic targets of the neuron through the generation of a distinctive burst of action potential output (Lisman, 1997).

Calcium spikes may serve as powerful regulators of synaptic plasticity, because they would likely mediate a substantial influx of calcium through voltage-gated calcium channels. Furthermore, the prolonged depolarizations mediated by calcium spikes would relieve the voltage-dependent block on NMDA receptors and induce additional calcium influx. Calcium spikes could thus serve as a robust cellular mechanism by which synaptic inputs conveying temporally correlated information might be selectively reinforced.


Andreasen M, Lambert JD (1995) Regenerative properties of pyramidal cell dendrites in area CA1 of the rat hippocampus. J Physiol (Lond) 483:421– 441.

Benardo LS, Masukawa LM, Prince DA (1982) Electrophysiology of isolated hippocampal pyramidal dendrites. J Neurosci 2:1614 –1622.

Kamondi A, Acsady L, Buzsa´ki G (1998) Dendritic spikes are enhanced by cooperative network activity in the intact hippocampus. J Neurosci 18:3919 –3928.

Lisman JE (1997) Bursts as a unit of neural information: making unreliable synapses reliable. Trends Neurosci 20:38–43.

Wong RK, Prince DA, Basbaum AI (1979) Intradendritic recordings from hippocampal neurons. Proc Natl Acad Sci USA 76:986 –990.

Wong RKS, Stewart M (1992) Different firing patterns generated in dendrites and somata of CA1 pyramidal neurones in guinea-pig hippocampus. J Physiol (Lond) 457:675– 687.

Anmerkungen

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[Calcium spikes could thus serve as a robust cellular mechanism by which synaptic inputs conveying temporally correlated information] might be selectively reinforced. This mechanism would be expected to function effectively in distal dendritic regions in which the influence of back propagating action potentials is comparatively weak (Spruston et al., 1995; Kamondi et al., 1998).

• Kamondi A, Acsády L, Buzsáki G (1998) Dendritic spikes are enhanced by cooperative network activity in the intact hippocampus. J Neurosci 18:3919-28.

• Spruston N, Schiller Y, Stuart G, Sakmann B (1995) Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites. Science 268:297-300.

Calcium spikes could thus serve as a robust cellular mechanism by which synaptic inputs conveying temporally correlated information might be selectively reinforced. This mechanism would be expected to function effectively in distal dendritic regions in which the influence of backpropagating action potentials is comparatively weak (Spruston et al., 1995; Kamondi et al., 1998).

Kamondi A, Acsady L, Buzsa´ki G (1998) Dendritic spikes are enhanced by cooperative network activity in the intact hippocampus. J Neurosci 18:3919–3928.

Spruston N, Schiller Y, Stuart G, Sakmann B (1995) Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites. Science 268:297–300.

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Among the spectrum of experimental strategies used by neurobiologists to promote the understanding of brain function, the in vitro systems offer a number of opportunities. In in vitro studies a large number of well-defined independent variables can be readily introduced. The dependent variables are usually more accessible to measurement and can be monitored with a variety of techniques than in the case of in vivo. The interference from peripheral factors, which are more common in in vivo is greatly reduced (Lynch, 1980).

[In our studies we are performing in vitro experiments with slices from hippocampus.] The main reason is because it contains a considerable proportion of the major fibre projections and their attendant synaptic domains can be prepared. Most of the major intrinsic and extrinsic hippocampal fibre systems are organized according to a lamellar plan in which they travel at right angles to the longitudinal axis of the structure (Anderson et al., 1971, Blackstad et al., 1970).


• Andersen P, Bliss TV, Lomo T, Olsen LI, Skrede KK (1969) Lamellar organization of hippocampal excitatory pathways. Acta Physiol Scand 76:4A-5.

• Blackstad TW, Brink K, Hem J, Jeune B (1970) Distribution of hippocampal mossy fibers in the rat. An experimental study with silver impregnation methods. J Comp Neurol.138:433-49.

• Lynch G, Schubert P (1980) The use of in vitro brain slices for multidisciplinary studies of synaptic function. Annu Rev Neurosci 3:1-22.

[Seite 1]

Among the spectrum of experimental strategies used by neurobiologists to promote the understanding of brain function, the in vitro approach has found a wide and constantly growing application. In vitro systems offer a number of opportunities not available with more conventional techniques:

1. a large number of well-defined independent variables can be readily introduced,

2. dependent variables are usually more accessible to measurement and can be monitored with a greater variety of techniques than is the case in vivo,

3. interference from peripheral factors, which often compromises in vivo experiments, is greatly reduced.

[Seite 3]

Finally, and most important, hippocampal slices that contain a considerable proportion of the major fiber projections and their attendant synaptic domains can be prepared. Most of the major intrinsic and extrinsic hippocampal fiber systems are organized according to a "lamellar" plan in which they travel at right angles to the longitudinal axis of the structure (Andersen et al 1971 b, Blackstad et al 1970).


Andersen, P., Bliss, T. V. P., Skrede, K. K. 1971 b. Lamellar organization of hippocampal excitatory pathways. Exp. Brain Res. 13:222-38

Blackstad, T. W., Brink, K., Hem, J., Jeune, B. 1970. Distribution of hippocampal mossy fibers in the rat: An experimental study with silver impregnation methods. J. Camp. Neural. 138;433-50

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The hippocampal slice offers a variety of opportunities like visual control of electrode placement, possibility to direct electrodes to known parts of a given cell. For example 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 population of synapses. Furthermore in the slice preparation, the ability to change the concentration of interesting molecules at will provides a 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. Brain slices offer a variety of novel opportunities, the most obvious being visual inspection. [...] 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. [...] 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.
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1.3.1. Properties of LTP

As a result of brief high frequency stimulation, the LTP expressed in CA3-CA1 synapse of hippocampal region show some basic properties such as ‘inputspecificity’, ‘co-operativity’, ‘associativity’ and ‘late-associativity’ (Bear and Malenka, 1994; Bliss and Collingridge, 1993; Frey and Morris, 1997, 1998; Malenka and Bear, 2004). LTP is input-specific in general, which means those synapses who receive high frequency stimulation only will express LTP. This property of LTP is consistent with its involvement in memory formation. If the activation of one set of synapses leads to the simultaneous activation of all other synapses, even inactive ones, being potentiated, it would be difficult to activate selectively a particular sets of inputs, as is presumably required for learning and memory (Bliss and Collingridge, 1993).


• Bear MF, Malenka RC (1994) Synaptic plasticity: LTP and LTD. Curr Opin Neurobiol 4:38 9[sic]-399.

• Bliss TV, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361:31-39.

• Frey U, Morris RGM (1997) Synaptic tagging and long-term potentiation. Nature 385:533-536.

• Frey U, Morris RGM (1998a) Synaptic tagging: implications for latemaintenance of hippocampal long-term potentiation. Trends Neurosci 21:181-188.

• Frey U, Morris RGM (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts for late-LTP. Neuropharmacology 37:545-552.

• Malenka RC and Bear MF (2004) LTP and LTD: an embarrassment of riches. Neuron 44:5-21.

1.4. Basic properties of LTP and LTD

LTP and LTD at the Schaffer collaterals CA1 synapses share several common properties: like input-specificity, co-operativity, associativity and late-associativity (Bliss and Collingridge, 1993;Bear and Malenka, 1994;Malenka and Bear, 2004). LTP/LTD is input-specific, in the sense that it is restricted to the synapses which receive high-frequency stimulation (HFS) or low-frequency stimulation respectively (LFS) (Kelso and Brown, 1986;Lynch et al., 1977). This feature is consistent with its involvement in memory formation. If activation of one set of synapses led to the activation of all other synapses, even inactive ones-being potentiated or depressed, it would be difficult to selectively enhance particular sets of inputs, as is presumably required for learning and memory (Bliss and Collingridge, 1993).


Bear MF, Malenka RC (1994) Synaptic plasticity: LTP and LTD. Curr Opin Neurobiol 4: 389-399.

Bliss TV, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361: 31-39.

Kelso SR, Brown TH (1986) Differential conditioning of associative synaptic enhancement in hippocampal brain slices. Science 232: 85-87.

Lynch GS, Dunwiddie T, Gribkoff V (1977) Heterosynaptic depression: a postsynaptic correlate of long-term potentiation. Nature 266: 737-739.

Malenka RC, Bear MF (2004) LTP and LTD; An Embarrassment of Riches. Neuron 44: 5-21.

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This selective enhancement of conjointly activated synaptic inputs is often considered as a cellular analog correlate of associative or classical conditioning. Otherways, associativity is expected in any network of neurons that links one set information with another. ‘Late-associativity’ is a novel property of LTP, which describes intersynaptic interventions within a time frame of few minutes to few hours (Frey and Morris, 1997, 1998a, 1998b). More clearly, a weak protein synthesis-independent early-LTP in one synaptic input can be [transformed into a late, protein synthesis-dependent form, if a protein synthesis-dependent late-LTP is induced in the second synaptic input preceded by the weak events in the first synaptic input (“Weak before strong”) within a specific time frame (Frey and Morris, 1998a, 1998b; Frey , 2001 ; Frey and Frey, 2008; Kauderer and Kandel, 2000; Sajikumar and Frey, 2004a).]

• Frey U, Frey S, Schollmeier F, Krug M (1995) 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, Morris RGM (1997) Synaptic tagging and long-term potentiation. Nature 385:533-536.

• Frey U, Morris RGM (1998a) Synaptic tagging: implications for late maintenance of hippocampal long-term potentiation. Trends Neurosci 21:181-188.

• Frey U, Morris RGM (1998b) Weak before strong: dissociating synaptic tagging and plasticity-factor accounts for late-LTP. Neuropharmacology 37:545-552.

• Frey S, Bergado-Rosado J, Seidenbecher T, Pape HC, Frey JU (2001) Reinforcement of early long-term potentiation (early-LTP) in dentate gyrus by stimulation of the basolateral amygdala: heterosynaptic induction mechanisms of late-LTP. J Neurosci 21:3697-3703.

• Kauderer BS, Kandel ER (2000) Capture of a protein synthesis-dependent component of long-term depression. Proc Natl Acad Sci U S A.97:13342-7.

• Sajikumar S, Frey JU (2004) Resetting of synaptic tags is time-and activity-dependent in rat hippocampal CA1 in vitro. Neuroscience 129:503-507.

• Sajikumar S, Frey JU (2004) Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD. Neurobiol Learn Mem 82:12-25.

This selective enhancement /depression of conjointly activated sets of synaptic inputs is often considered as a cellular analog of associative or classical conditioning. More generally, associativity is expected in any network of neurons that links one set of information with another.

Late-associativity is a novel property of LTP/LTD. It describes intersynaptic interventions within a time frame of few minutes to few hours (Frey and Morris, 1997;Frey and Morris, 1998a;Frey and Morris, 1998b;Morris and Frey, 1999). More clearly, a weak protein synthesis independent early-LTP/-LTD in one synaptic input can be transformed into a late, protein synthesis-dependent form, if a protein synthesis-dependent late-LTP/-LTD is induced in the second synaptic input preceded by the weak events in the first synaptic input (weak before strong) within a specific time frame (Frey and Morris, 1998b;Kauderer and Kandel, 2000).


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.

Kauderer BS, Kandel ER (2000) Capture of a protein synthesis-dependent component of long-term depression. Proc Natl Acad Sci U S A 97: 13342-13347.

Morris RG, Frey U (1999) Tagging the hebb synapse: reply. Trends Neurosci 22: 256.

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Because the NMDA receptors are sensitive to both presynaptic transmitter release and postsynaptic depolarization; they act as Hebbian coincidence detectors (Collingridge, 2003). NMDA-receptor-dependent LTP can be triggered experimentally either by delivering high-frequency trains to a critical number of presynaptic afferents, or by [pairing postsynaptic depolarization with pre-synaptic stimulation (Wigstrom [sic] and Gustafsson, 1986).]

• Collingridge G (2003) The induction of N-methyl-D-aspartate receptordependent long-term potentiation. Philos Trans R Soc Lond B Biol Sci 358:635-41.

• Wigström H, Gustafsson B (1986) Postsynaptic control of hippocampal longterm potentiation. J Physiol (Paris) 81:228-36.

Because NMDA-receptors are sensitive to both presynaptic transmitter release and postsynaptic depolarization, they act as Hebbian coincidence detectors (Collingridge, 2003). NMDA-receptor- dependent LTP can be triggered experimentally either by delivering high-frequency tetani to a critical number of presynaptic afferent fibers, or by pairing postsynaptic depolarization with presynaptic stimulation (Gustafsson et al., 1987).

Collingridge GL (2003) The induction of N-methyl-D-aspartate receptor-dependent long-term potentiation. Philos Trans R Soc Lond B Biol Sci 358: 635-641.

Gustafsson B, Wigstrom H, Abraham WC, Huang YY (1987) Long-term potentiation in the hippocampus using depolarizing current pulses as the conditioning stimulus to single volley synaptic potentials. J Neurosci 7: 774-780.

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Though nearly identical nothing has been marked as a citation.

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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 the dura was removed before transferring the brain into cooled and carbogenated (carbogen: gas consisting of 95% O2 and 5% CO2) artificial cerebrospinal fluid (ACSF) (temperature 40C) (Reymann et al., 1985). 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). Cooling the petridish and tissue slicer support on ice may help to reduce tissue deterioration. Brain is placed in a petridish on filter paper and the cerebellum and frontal cortex is dissected away. Then the remaining part of the brain is divided 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 a manuel chopper (Cambden, UK). The hippocampus was chopped into 400μm thick slices at 700 angle 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 glass vessel containing the cooled and carbogenated ACSF, and immediately transferred to the nylon net in the experimental chamber maintained at 320C by a wide mouthed pipette.

• 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.

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). 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). Chilling the petridish and tissue slicer support on ice may help reduce tissue deterioration. Brain is placed in a petriplate on filter paper and the cerebellum and frontal cortex is dissected away. 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 32oC by a wide bored pipette.

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.

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Persistently active kinases meet several criteria for the tag, as they allow a synapse to remember previous activity in a spatially restricted and reversible manner. Calcium/calmodulin-dependent protein kinase II (CaMKII), which becomes autonomously and persistently active by autophosphorylation, has been activated by synaptic stimulation, meets an identity of the tag. [...] The atypical protein kinase C known as protein kinase M Zeta (PKMζ), the persistent activity of which requires protein synthesis, has been shown to be another possible candidate. Kinases. Persistently active kinases meet several of the criteria for a tag, as they allow a synapse to ‘remember’ previous activity in a spatially restricted and reversible manner. Calcium/calmodulin-dependent protein kinase II (CaMKII), which becomes autonomously and persistently active by autophosphorylation, has been shown to be activated by, and necessary for, long-term plasticity and long-term memory8. The atypical protein kinase C known as protein kinase Mζ (PKM-ζ), the persistent activity of which requires protein synthesis9, has been shown to be both necessary and sufficient for the maintenance of L-LTP in the hippocampus10.

8. Lisman, J., Schulman, H. & Cline, H. The molecular basis of CaMKII function in synaptic and behavioural memory. Nature Rev. Neurosci. 3, 175–190 (2002).

9. Osten, P., Valsamis, L., Harris, A. & Sacktor, T. C. Protein synthesis-dependent formation of protein kinase Mζ in longterm potentiation. J. Neurosci. 16, 2444–2451 (1996).

10. Ling, D. S. et al. Protein kinase Mζ is necessary and sufficient for LTP maintenance. Nature Neurosci. 5, 295–296 (2002).

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The CaMKII holoenzymes were shown to be capable of associating with one another in response to Ca2+ [sic].Therefore CaMKII may form a scaffold that, in combination with other synaptic proteins, recruits and localizes additional proteins to the postsynaptic density (Hudmon et al., 2005). The atypical protein kinase C known as protein kinase M Zeta (PKMζ), the persistent activity of which requires protein synthesis, has been shown to be another possible candidate. But recently it has [been found that PKMζ is the first LTP specific plasticity-related protein (PRP) and not a tag molecule in apical CA1 branches (Sajikumar et al., 2005) but in basal dendrites the coactivation of PKA or PKM Zeta is required for synaptic tagging (Sajikumar et al., 2007).]

• Hudmon A, Lebel E, Roy H, Sik A, Schulman H, Waxham MN, De Koninck P (2005) A mechanism for Ca2+/calmodulin-dependent protein kinase II clustering at synaptic and nonsynaptic sites based on self-association. J Neurosci 25:6971-83.

• Sajikumar S, Navakkode S, Frey JU (2005) Protein synthesis-dependent long-term functional plasticity: Methods and techniques. Curr Opin Neurobiol 15:607-613.

• Sajikumar S, Navakkode S, Sacktor TC, Frey JU (2005b) Synaptic tagging and cross tagging: the role of protein kinase M zeta in maintaining long-term potentiation but not long-term depression. J Neurosci 25:5750-5756.

[page 37]

The atypical protein kinase C known as protein kinase Mζ (PKMζ), the persistent activity of which requires protein synthesis, has been shown to be another possible candidate. But recently we could identify PKMæ as the first LTP specific plasticity related protein, not a tag molecule (Sajikumar et al., 2005b).

[page 90]

More recently Hudmon et al showed that CaMKII holoenzymes were shown to be capable of associating with one another (or self-associate) in response to Ca2+ stimulation. Therefore CaMKII may form a scaffold that, in combination with other synaptic proteins, recruits and localizes additional proteins to the postsynaptic density. They also discussed the potential function of CaMKII self-association as a ´tag´ of synaptic activity (Hudmon et al., 2005). [...]


74. Hudmon A, Lebel E, Roy H, Sik A, Schulman H, Waxham MN, De Koninck P (2005) A mechanism for Ca2+/calmodulin-dependent protein kinase II clustering at synaptic and nonsynaptic sites based on self-association. J Neurosci 25: 6971-6983.

139. Sajikumar S, Navakkode S, Frey JU (2005a) Protein synthesis-dependent long-term functional plasticity: methods and techniques. Curr Opin Neurobiol ..

140. Sajikumar S, Navakkode S, Sacktor TC, Frey JU (2005b) Synaptic tagging and cross-tagging: the role of protein kinase Mzeta in maintaining long-term potentiation but not long-term depression. J Neurosci 25: 5750-5756.

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From the final part - "Discussion" - of the thesis, Not marked as a citation.

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The local activation of PKA and local regulation of ubiquitin-proteosome pathway can serve as synaptic tag that combine with transcriptional events to produce persistent and local synaptic strengthening (Chain et al., 1999; Hegde et al., 1997; Schwartz et al., 1999).

Changes in adhesion molecule are likely to underlie the morphological changes that are associated with synaptic strengthening (Kandel et al., 1993). In consistent with the idea that cell adhesion molecule dynamics could serve as synaptic tags, alterations in cell adhesion molecule at the synapse have been found to occur during many form of the synaptic plasticity. [...] They [the cadherins] have been shown to dimerize and alter their conformation during depolarization (Tanaka et al., 2000).

Another potential candidate for a synaptic tag that has recently received significant attention is the actin micro filament network at the synapse. The actin network in neurons is extremely dynamic, and these dynamics have been shown to change with activity (Matus et al., 2000; Murthy et al., 2001). Changes in the actin cytoskeleton probably accompany changes in cell-adhesion molecules, as most adhesion molecules are linked to the actin cytoskeleton. In addition, changes in the actin microfilament network are likely to underlie the growth of new synaptic structures that have been observed after repetitive stimulation of hippocampal synapses (Engert et al., 1999; Muller et al., 1999; Svoboda et al., 1999).


• Bailey CH, Kandel ER (1993) Structural changes accompanying memory storage. Annu Rev Physiol 55:397-426.

• Bozdagi O, Shan W, Tanaka H, Benson DL, Huntley GW (2000) Increasing numbers of synaptic puncta during late-phase LTP: N-cadherin is synthesized, recruited to synaptic sites, and required for potentiation. Neuron 28:245-59.

• Engert F, Bonhoeffer T (1999) Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature 399:66-70.

• Matus A (2000) Actin based plasticity in dendritic spines. Science 290:754-758.

• Muller RU, Poucet B, Fenton AA, Cressant A (1999) Is the hippocampus of the rat part of a specialized navigational system? Hippocampus 9:413-22.

• Star EN, Kwiatkowski DJ, Murthy VN (2002) Rapid turnover of actin in dendritic spines and its regulation by activity.Nat Neurosci 5:239-46.

• Svoboda K, Helmchen F, Denk W, Tank DW (1999) Spread of dendritic excitation in layer 2/3 pyramidal neurons in rat barrel cortex in vivo. Nat Neurosci 2:65-73.

[Seite 815]

Together, these findings raise the possibility that local activation of

[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.

Adhesion molecules. Changes in adhesion are likely to underlie the morphological changes that are associated with synaptic strengthening16. [...]

Consistent with the idea that adhesion-molecule dynamics could serve as synaptic tags, alterations in cell-adhesion molecules at the synapse have been found to occur during many forms of synaptic plasticity. [...] Also, the cadherins have been shown to dimerize and alter their conformation during depolarization22, and the number of cadherin-positive synapses has been shown to increase in a protein-synthesis-dependent manner during LTP23. [...]

Actin network. 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. Changes in the actin cytoskeleton probably accompany changes in cell-adhesion molecules, as most adhesion molecules are linked to the cytoskeleton. In addition, changes in the actin microfilament network are likely to underlie the growth of new synaptic structures that has been observed after repetitive stimulation of hippocampal synapses29–31 and after serotonergic stimulation of Aplysia sensorimotor connections32.


16. Bailey, C. H. & Kandel, E. R. Structural changes accompanying memory storage. Annu. Rev. Physiol. 55, 397–426 (1993).

22. Tanaka, H. et al. Molecular modification of N-cadherin in response to synaptic activity. Neuron 25, 93–107 (2000).

23. Bozdagi, O., Shan, W., Tanaka, H., Benson, D. L. & Huntley, G. W. Increasing numbers of synaptic puncta during late-phase LTP: N-cadherin is synthesized, recruited to synaptic sites, and required for potentiation. Neuron 28, 245–259 (2000).

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).

29. Engert, F. & Bonhoeffer, T. Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature 399, 66–70 (1999).

30. Maletic-Savatic, M., Malinow, R. & Svoboda, K. Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity. Science 283, 1923–1927 (1999).

31. Toni, N., Buchs, P. A., Nikonenko, I., Bron, C. R. & Muller, D. LTP promotes formation of multiple spine synapses between a single axon terminal and a dendrite. Nature 402, 421–425 (1999).

Anmerkungen

Im Diskussionsteil. Ohne Hinweis auf eine Übernahme.

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(Graf Isolan) Schumann

[23.] Br/Fragment 077 01 - Diskussion
Bearbeitet: 21. May 2016, 17:49 Schumann
Erstellt: 31. December 2013, 13:19 (Graf Isolan)
Br, Fragment, Gesichtet, Martin und Kosik 2002, SMWFragment, Schutzlevel sysop, Verschleierung

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[The stimuli that can produce a synaptic tag are not necessarily sufficient to activate protein synthesis, and are therefore frequently considered to be sub]threshold for long-term plasticity. Such stimuli induce a host of changes at the synapse and any number of these changes could potentially serve as a tag. Many of these changes are related to the activity and strength of the synapse, such as rapid addition of AMPA receptors to ionotropic glutamate receptor clusters (Shi et al., 1999), the lateral mobility of NMDA receptors between synaptic and extra-synaptic sites (Westbrook et al., 2002) etc. Such events could serve as localized traces of previous synaptic activity that are able to produce synaptic strengthening on their own with in [sic] a limited time period. However, to function as synaptic tags, they would need to be able to interact with cell wide events to produce local and persistent increase in synaptic efficacy.

• Shi SH, Hayashi Y, Petralia RS, Zaman SH, Wenthold RJ, Svoboda K, Malinow R (1999) Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation. Science 284:1811-6.

The stimuli that can produce a synaptic tag are not necessarily sufficient to activate transcription, and are therefore frequently considered to be subthreshold for long-term plasticity. [...] Such stimuli induce a host of changes at the synapse, and any number of these changes could potentially serve as a tag. Many of these changes are related to the activity and strength of the synapse, such as the rapid addition of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors to ionotropic glutamate receptor clusters4, the lateral mobility of NMDA (N-methyl-D-aspartate) receptors between synaptic and extrasynaptic sites5, [HOMER-mediated insertion of the metabotropic glutamate receptor mGluR5 into the membrane6, and palmitate cycling on postsynaptic density protein 95 (PSD95; REF. 7)]. Such events could serve as localized traces of previous synaptic activity that are able to produce synaptic strengthening on their own within a limited time period. However, to function as synaptic tags, they would need to be able to interact with cell-wide events to produce local and persistent increases in synaptic efficacy.

4. Shi, S. H. et al. Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation. Science 284, 1811–1816 (1999).

5. Tovar, K. R. & Westbrook, G. L. Mobile NMDA receptors at hippocampal synapses. Neuron 34, 255–264 (2002).

[6. Ango, F. et al. Homer-dependent cell surface expression of metabotropic glutamate receptor type 5 in neurons. Mol. Cell. Neurosci. 20, 323–329 (2002).

7. El-Husseini, A. E. et al. Synaptic strength regulated by palmitate cycling on PSD-95. Cell 108, 849–863 (2002).]

Anmerkungen

Im Diskussionsteil. Ohne Hinweis auf eine Übernahme.

Für die Quelle "(Westbrook et al., 2002)" findet sich im Literaturverzeichnis von Br keine Referenz.

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