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Angaben zur Quelle [Bearbeiten]

Autor     Michael Makhinson, Jennifer K. Chotiner, Joseph B. Watson, Thomas J. O’Dell
Titel    Adenylyl Cyclase Activation Modulates Activity-Dependent Changes in Synaptic Strength and Ca2+/Calmodulin-Dependent Kinase II Autophosphorylation
Zeitschrift    The Journal of Neuroscience
Datum    1. April 1999
Jahrgang    19
Nummer    7
Seiten    2500-2510
URL    http://www.jneurosci.org/content/19/7/2500.full.pdf

Literaturverz.   

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Fußnoten    nein
Fragmente    2


Fragmente der Quelle:
[1.] Sng/Fragment 023 04 - Diskussion
Zuletzt bearbeitet: 2016-05-22 22:02:19 Schumann
Fragment, Gesichtet, KomplettPlagiat, Makhinson et al 1999, SMWFragment, Schutzlevel sysop, Sng

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KomplettPlagiat
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Graf Isolan
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Untersuchte Arbeit:
Seite: 23, Zeilen: 4-16
Quelle: Makhinson et al 1999
Seite(n): 2507-2508, Zeilen: 2507:re.Sp. 47-62 - 2508:li.Sp. 1-2
The Lisman model of LTP (Lisman and McIntyre, 2001) proposes that patterns of synaptic activity that produce low levels of NMDA receptor activation and small increase in intracellular Ca2+ depress synaptic strength via a cascade of protein phosphatase activation (Mulkey et al., 1993). This cascade of protein phosphatase activation is thought to entail a Ca2+- and calmodulin-dependent activation of calcineurin, that dephosphorylates the PP1 regulatory protein inhibitor-1 (Mulkey et al., 1994). Dephosphorylation of inhibitor-1 activates PP1 that in turn dephosphorylates CaMKII. In contrast, stronger levels of NMDA receptor activation and larger increase in intracellular Ca2+ induce LTP by increasing levels of autophosphorylated CaMKII via a simultaneous activation of CaMKII and downregulation of PP1. In the model, a large increase in Ca2+ is thought to suppress PP1 activation by stimulating Ca2+- and calmodulin-sensitive isoforms of adenylate cyclase (AC) and by activating PKA that suppresses PP1 activation by opposing calcineurin-mediated dephosphorylation of inhibitor-1.

94. Lisman JE, McIntyre CC (2001) Synaptic plasticity: a molecular memory switch. Curr Biol 11: R788-R791.

110. Mulkey RM, Endo S, Shenolikar S, Malenka RC (1994) Involvement of a calcineurin/inhibitor-1 phosphatase cascade in hippocampal long-term depression. Nature 369: 486-488.

111. Mulkey RM, Herron CE, Malenka RC (1993) An essential role for protein phosphatases in hippocampal long-term depression. Science 261: 1051-1055.

[Seite 2507]

The Lisman model of LTP (Lisman, 1994) proposes that patterns of synaptic activity that produce low levels of NMDA receptor activation and small increases in intracellular Ca2+ depress synaptic strength via a cascade of protein phosphatase activation (Mulkey and Malenka, 1992; Mulkey et al., 1993, 1994). This cascade of protein phosphatase activation is thought to entail a Ca2+- and calmodulin-dependent activation of calcineurin that dephosphorylates the PP1 regulatory protein inhibitor-1 (Mulkey et al., 1994). Dephosphorylation of inhibitor-1 activates PP1 that in turn dephosphorylates CaMKII. In contrast, stronger levels of NMDA receptor activation and larger increases in intracellular Ca2+ induce LTP by increasing levels of autophosphorylated CaMKII via a simultaneous activation of CaMKII and downregulation of PP1. In the model, a large increase in Ca2+ is thought to suppress PP1 activation by stimulating Ca2+- and calmodulin-sensitive isoforms of AC and by

[Seite 2508]

activating PKA that suppresses PP1 activation by opposing calcineurin-mediated dephosphorylation of inhibitor-1.


Lisman JE (1994) The CaM kinase II hypothesis for the storage of synaptic memory. Trends Neurosci 17:406–412.

Mulkey RM, Malenka RC (1992) Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus. Neuron 9:967–975.

Mulkey RM, Herron CE, Malenka RC (1993) An essential role for protein phosphatases in hippocampal long-term depression. Science 261:1051–1055.

Mulkey RM, Endo S, Shenolikar A, Malenka RC (1994) Involvement of a calcineurin/inhibitor-1 phosphatase cascade in hippocampal longterm depression. Nature 369:486–488.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[2.] Sng/Fragment 024 14 - Diskussion
Zuletzt bearbeitet: 2016-05-22 22:05:05 Schumann
Fragment, Gesichtet, Makhinson et al 1999, SMWFragment, Schutzlevel sysop, Sng, Verschleierung

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Untersuchte Arbeit:
Seite: 24, Zeilen: 14-21
Quelle: Makhinson et al 1999
Seite(n): 2508, Zeilen: li.Sp. 53-62
Though PKA was initially identified as having an important signaling role in the protein synthesis-dependent late stages of LTP (Frey et al., 1993), more recent evidence suggests that PKA also provides a mechanism for suppression of protein phosphatase activation in the early stages of LTP induction (Blitzer et al., 1995;Winder et al., 1998;Blitzer et al., 1998). Activation of the cAMP-PKA signaling pathway regulates both activity-dependent changes in synaptic strength and CaMKII phosphorylation in a chemical LTP induction protocol (Yamamori et al., 2004).

23. Blitzer RD, Connor JH, Brown GP, Wong T, Shenolikar S, Iyengar R, Landau EM (1998) Gating of CaMKII by cAMP-regulated protein phosphatase activity during LTP. Science 280: 1940-1942.

24. Blitzer RD, Wong T, Nouranifar R, Iyengar R, Landau EM (1995) Postsynaptic cAMP pathway gates early LTP in hippocampal CA1 region. Neuron 15: 1403-1414.

54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664.

171. Winder DG, Mansuy IM, Osman M, Moallem TM, Kandel ER (1998) Genetic and pharmacological evidence for a novel, intermediate phase of long-term potentiation suppressed by calcineurin. Cell 92: 25-37.

174. Yamamori E, Asai M, Yoshida M, Takano K, Itoi K, Oiso Y, Iwasaki Y (2004) Calcium/calmodulin kinase IV pathway is involved in the transcriptional regulation of the corticotropin-releasing hormone gene promoter in neuronal cells. J Mol Endocrinol 33: 639-649.

Although PKA was initially identified as having an important signaling role in the protein synthesis-dependent late stages of LTP (Frey et al., 1993; Matthies and Reymann, 1993), more recent evidence suggests that PKA also provides a mechanism for suppression of protein phosphatase activation in the early stages of LTP induction (Blitzer et al., 1995, 1998; Thomas et al., 1996; Winder et al., 1998). Consistent with this notion, our results show that activation of the cAMP–PKA signaling pathway regulates both activity-dependent changes in synaptic strength and CaMKII phosphorylation in a chemLTP induction protocol.

Blitzer RD, Wong T, Nouranifar R, Iyengar R, Landau EM (1995) Postsynaptic cAMP pathway gates early LTP in the hippocampal CA1 region. Neuron 15:1403–1414.

Blitzer RD, Connor JH, Brown GP, Wong T, Shenolikar S, Iyengar R, Landau EM (1998) Gating of CaMKII by cAMP-regulated protein phosphatase activity during LTP. Science 280:1940 –1943.

Frey U, Huang Y-Y, Kandel ER (1993) Effects of cAMP simulate a late phase of LTP in hippocampal CA1 neurons. Science 260:1661–1664.

Matthies H, Reymann KG (1993) Protein kinase A inhibitors prevent the maintenance of hippocampal long-term potentiation. NeuroReport 4:712–714.

Thomas MJ, Moody TD, Makhinson M, O’Dell TJ (1996) Activity-dependent b-adrenergic modulation of low frequency stimulation induced LTP in the hippocampal CA1 region. Neuron 17:475– 482.

Winder DG, Mansuy IM, Osman M, Moallem TM, Kandel ER (1998) Genetic and pharmacological evidence for a novel, intermediate phase of long-term potentiation suppressed by calcineurin. Cell 92:25–37.

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Sichter
(Graf Isolan) Schumann

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