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Angaben zur Quelle [Bearbeiten]

Autor     Kelsey C. Martin und Kenneth S. Kosik
Titel    Synaptic Tagging - Who's it?
Zeitschrift    Nature Reviews Neuroscience
Datum    Oktober 2002
Nummer    3
Seiten    813-820
DOI    10.1038/nrn942
URL    http://www.nature.com/nrn/journal/v3/n10/abs/nrn942.html, http://www.researchgate.net/publication/11097967_Synaptic_tagging_--_who's_it/file/9fcfd507effbec3c58.pdf

Literaturverz.   

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Fußnoten    nein
Fragmente    3


Fragmente der Quelle:
[1.] Br/Fragment 075 16 - Diskussion
Zuletzt bearbeitet: 2016-05-21 17:51:11 Schumann
Br, Fragment, Gesichtet, Martin und Kosik 2002, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 75, Zeilen: 16-21, 24-26
Quelle: Martin und Kosik 2002
Seite(n): 815, Zeilen: re.Sp. 34-45
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).

Anmerkungen

Im Diskussionsteil. Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[2.] Br/Fragment 076 04 - Diskussion
Zuletzt bearbeitet: 2016-05-21 17:47:34 Schumann
Br, Fragment, Gesichtet, Martin und Kosik 2002, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 76, Zeilen: 4-12, 14-24
Quelle: Martin und Kosik 2002
Seite(n): 815-816, Zeilen: 815:re.Sp.: letzte Zeile - 816: li.Sp. 1-8.27-30.35-37.54-59 - re.Sp. 1-6
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.

Sichter
(Graf Isolan) Schumann

[3.] Br/Fragment 077 01 - Diskussion
Zuletzt bearbeitet: 2016-05-21 17:49:30 Schumann
Br, Fragment, Gesichtet, Martin und Kosik 2002, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
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Quelle: Martin und Kosik 2002
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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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