102
Views
1
CrossRef citations to date
0
Altmetric
Original Articles

Oligomeric Aβ25–35 induces the tyrosine phosphorylation of PSD-95 by SrcPTKs in rat hippocampal CA1 subfield

, &
Pages 888-895 | Received 10 Sep 2020, Accepted 11 Nov 2021, Published online: 09 Dec 2021

References

  • Knowles TP, Vendruscolo M, Dobson CM. The amyloid state and its association with protein misfolding diseases. Nat Rev Mol Cell Biol. 2014;15(6):384–396.
  • Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991;82(4):239–259.
  • Selkoe DJ, Hardy J. The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Mol Med. 2016;8(6):595–608.
  • Rajasekhar K, Chakrabarti M, Govindaraju T. Function and toxicity of amyloid beta and recent therapeutic interventions targeting amyloid beta in Alzheimer’s disease. Chem Commun (Camb)). 2015;51(70):13434–13450.
  • Sengupta U, Nilson AN, Kayed R. The role of amyloid-β oligomers in toxicity, propagation, and immunotherapy. EBioMedicine. 2016;6:42–49.
  • Tu S, Okamoto S, Lipton SA, et al. Oligomeric Aβ-induced synaptic dysfunction in Alzheimer’s disease. Mol Neurodegener. 2014;9:48.
  • Reiss AB, Arain HA, Stecker MM, et al. Amyloid toxicity in Alzheimer’s disease. Rev Neurosci. 2018;29(6):613–627.
  • Selkoe DJ. Soluble oligomers of the amyloid β-protein impair synaptic plasticity and behavior. Behav Brain Res. 2008;192(1):106–113.
  • Haass C, Selkoe DJ. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat Rev Mol Cell Biol. 2007;8(2):101–112.
  • Klementiev B, Novikova TV, Walmod P, et al. A neural cell adhesion molecule-derived peptide reduces neuropathological signs and cognitive impairment induced by Aβ25–35. Neuroscience. 2007;145(1):209–224.
  • Zhou F, Xu Y, Hou XY. MLK3-MKK3/6-P38MAPK Cascades following NMDA receptor activation contributes to amyloid-peptide-induced apoptosis in SH-SY5Y cells. J Neurosci Res. 2014;92(6):808–817.
  • Xu Y, Cao DH, Wu GM, et al. Involvement of P38MAPK activation by NMDA receptors and non-NMDA receptors in amyloid-β peptide-induced neuronal loss in rat hippocampal CA1 and CA3 subfields. Neurosci Res. 2014;85:51–57.
  • Ball MJ. Neuronal loss, neurofibrillary tangles and grancelovascular degeneration in the hippocampus with aging and dementia. Acta Neuropathol. 1977;37(2):111–118.
  • Hrynchak MV, Rierola M, Golovyashkina N, et al. Chronic presence of oligomeric Aβ differentially modulates spine parameters in the hippocampus and cortex of mice with low APP transgene expression. Front Synaptic Neurosci. 2020;12:16.
  • Wu GM, Hou XY. Oligomerized Aβ25–35 induces increased tyrosine phosphorylation of NMDA receptor subunit 2A in rat hippocampal CA1 subfield. Brain Res. 2010;1343:186–193.
  • Koppensteiner P, Trinchese F, Fà M, et al. Time-dependent reversal of synaptic plasticity induced by physiological concentrations of oligomeric Aβ42: an early index of Alzheimer’s disease. Sci Rep. 2016;6:32553.
  • Sheng M, Hoogenraad CC. The postsynaptic architecture of excitatory synapses: a more quantitative view. Annu Rev Biochem. 2007;76:823–847.
  • Kim E, Sheng M. PDZ domain proteins of synapses. Nat Rev Neurosci. 2004;5(10):771–781.
  • Kalia LV, Salter MW. Interactions between Src family protein tyrosine kinases and PSD-95. Neuropharmacology. 2003;45(6):720–728.
  • Du CP, Gao J, Tai JM, et al. Increased tyrosine phosphorylation of PSD-95 by Src family kinases after brain ischaemia. Biochem J. 2009;417(1):277–285.
  • Zhao C, Du CP, Peng Y, et al. The upregulation of NR2A-containing N-methyl-D-aspartate receptor function by tyrosine phosphorylation of postsynaptic density 95 via facilitating Src/proline-rich tyrosine kinase 2 activation. Mol Neurobiol. 2015;51(2):500–511.
  • Ali DW, Salter MW. NMDA receptor regulation by Src kinase signalling in excitatory synaptic transmission and plasticity. Curr Opin Neurobiol. 2001;11(3):336–342.
  • Ohnishi H, Murata Y, Okazawa H, et al. Src family kinases: modulators of neurotransmitter receptor function and behavior. Trends Neurosci. 2011;34(12):629–637.
  • Salter MW. Src, N-methyl-D-aspartate (NMDA) receptors, and synaptic plasticity. Biochem Pharmacol. 1998;56(7):789–798.
  • Lim SL, Tran DN, Zumkehr J, et al. Inhibition of hematopoietic cell kinase dysregulates microglial function and accelerates early stage Alzheimer’s disease-like neuropathology. Glia. 2018;66(12):2700–2718.
  • Yuan Xiang P, Janc O, Grochowska KM, et al. Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases. Neurobiol Aging. 2016;40:98–102.
  • Köhr G. NMDA receptor function: subunit composition versus spatial distribution. Cell Tissue Res. 2006;326(2):439–446.
  • Iwamoto T, Yamada Y, Hori K, et al. Differential modulation of NR1-NR2A and NR1-NR2B subtypes of NMDA receptor by PDZ domain-containing proteins. J Neurochem. 2004;89(1):100–108.
  • Lin Y, Skeberdis VA, Francesconi A, et al. Postsynaptic density protein-95 regulates NMDA channel gating and surface expression. J Neurosci. 2004;24(45):10138–10148.
  • Roselli F, Tirard M, Lu J, et al. Soluble beta-amyloid1–40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses. J Neurosci. 2005;25(48):11061–11070.
  • Li S, Hong S, Shepardson NE, et al. Soluble oligomers of amyloid beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake. Neuron. 2009;62(6):788–801.
  • Niethammer M, Kim E, Sheng M. Interaction between the C terminus of NMDA receptor subunits and multiple members of the PSD-95. J Neurosci. 1996;16(7):2157–2163.
  • Hynd MR, Scott HL, Dodd PR. Glutamate-mediated excitotoxicity andneurodegeneration in Alzheimer’s disease. Neurochem Int. 2004;45(5):583–595.
  • Du CP, Tan R, Hou XY. Fyn kinases play a critical role in neuronal apoptosis induced by oxygen and glucose deprivation or amyloid-β peptide treatment. CNS Neurosci Ther. 2012;18(9):754–761.
  • Shao CY, Mirra SS, Sait HB, et al. Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer’s disease. Acta Neuropathol. 2011;122(3):285–292.
  • Wong TP, Marchese G, Casu MA, et al. Loss of presynaptic and postsynaptic structures is accompanied by compensatory increase in action potential-dependent synaptic input to layer V neocortical pyramidal neurons in aged rats. J Neurosci. 2000;20(22):8596–8606.
  • Kalia LV, Gingrich JR, Salter MW. Src in synaptic transmission and plasticity. Oncogene. 2004;23(48):8007–8016.
  • Zheng CY, Seabold GK, Horak M, et al. MAGUKs, synaptic development, and synaptic plasticity. Neuroscientist. 2011;17(5):493–512.
  • Bartos JA, Ulrich JD, Li H, et al. Postsynaptic clustering and activation of Pyk2 by PSD-95. J Neurosci. 2010;30(2):449–463.
  • Salazar SV, Cox TO, Lee S, et al. Alzheimer’s disease risk factor Pyk2 mediates amyloid-β-induced synaptic dysfunction and loss. J Neurosci. 2019;39(4):758–772.
  • Xu Y, Hou XY, Liu Y, et al. Different protection of K252a and N-acetyl-L-cysteine against amyloid-beta peptide-induced cortical neuron apoptosis involving inhibition of MLK3-MKK7-JNK3 signal Cascades. J Neurosci Res. 2009;87(4):918–927.
  • Savinainen A, Garcia EP, Dorow D, et al. Kainate receptor activation induces mixed lineage kinase-mediated cellular signaling Cascades via post-synaptic density protein 95. J Biol Chem. 2001;276(14):11382–11386.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.