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| [1.] Sng/Fragment 024 01 - Diskussion Zuletzt bearbeitet: 2016-05-22 22:06:20 Schumann | Blitzer et al 2005, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Sng, Verschleierung |
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Quelle: Blitzer et al 2005 Seite(n): 115, Zeilen: Legende zu Figure 2 |
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| 1.6.3. The interaction of three major postsynaptic signaling pathways in LTP
Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3′,5′-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP (Frey et al., 1993;English and Sweatt, 1997;Bortolotto and Collingridge, 1998). The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation (Giovannini et al., 2001). PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase (Atkins et al., 2005). 15. Atkins CM, Davare MA, Oh MC, Derkach V, Soderling TR (2005) Bidirectional regulation of cytoplasmic polyadenylation element-binding protein phosphorylation by Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 1 during hippocampal long-term potentiation. J Neurosci 25: 5604-5610. 26. Bortolotto ZA, Collingridge GL (1998) Involvement of calcium/calmodulin-dependent protein kinases in the setting of a molecular switch involved in hippocampal LTP. Neuropharmacology 37: 535-544. 47. English JD, Sweatt JD (1997) A requirement for the mitogen-activated protein kinase cascade in hippocampal long term potentiation. J Biol Chem 272: 19103-19106. 54. Frey U, Huang YY, Kandel ER (1993) Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons. Science 260: 1661-1664. 64. Giovannini MG, Blitzer RD, Wong T, Asoma K, Tsokas P, Morrison JH, Iyengar R, Landau EM (2001) Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation. J Neurosci 21: 7053-7062. |
Figure 2. The interaction of three major postsynaptic signaling pathways in LTP. Ca2+/calmodulin protein kinase II (CaMKII), mitogen-activated protein kinase (MAPK), and adenosine 3’,5’-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) are all required for the induction of LTP. The influx of Ca2+ through N-methyl-D-aspartate-type receptors (NMDA-R) or voltage-dependent Ca2+ channels (VDCC) can engage signaling cascades that activate these kinases, and PKA can additionally be activated by β-adrenergic receptors (β-AR) and other G protein-coupled receptors. MAPK and CaMKII can promote the phosphorylation of each other, and MAPK is required for an increase in CaMKII levels produced by LTP-inducing stimulation. PKA activity promotes CaMKII phosphorylation by indirectly inhibiting the protein phosphatase PP1, which would otherwise limit the degree or persistence of CaMKII activation by dephosphorylating the kinase. |
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| [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 |
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| 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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