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Items: 1 to 20 of 75

1.

Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression.

Kessels HW, Nabavi S, Malinow R.

Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):4033-8. doi: 10.1073/pnas.1219605110. Epub 2013 Feb 19.

2.

Amyloid beta peptide 1-42 disturbs intracellular calcium homeostasis through activation of GluN2B-containing N-methyl-d-aspartate receptors in cortical cultures.

Ferreira IL, Bajouco LM, Mota SI, Auberson YP, Oliveira CR, Rego AC.

Cell Calcium. 2012 Feb;51(2):95-106. doi: 10.1016/j.ceca.2011.11.008. Epub 2011 Dec 15.

PMID:
22177709
3.

Calcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic loss.

Birnbaum JH, Bali J, Rajendran L, Nitsch RM, Tackenberg C.

Cell Death Dis. 2015 Jun 18;6:e1791. doi: 10.1038/cddis.2015.160.

4.

Altered GluN2B NMDA receptor function and synaptic plasticity during early pathology in the PS2APP mouse model of Alzheimer's disease.

Hanson JE, Pare JF, Deng L, Smith Y, Zhou Q.

Neurobiol Dis. 2015 Feb;74:254-62. doi: 10.1016/j.nbd.2014.11.017. Epub 2014 Dec 4.

5.

Differential Regulation of N-Methyl-D-Aspartate Receptor Subunits is an Early Event in the Actions of Soluble Amyloid-β(1-40) Oligomers on Hippocampal Neurons.

Chang L, Zhang Y, Liu J, Song Y, Lv A, Li Y, Zhou W, Yan Z, Almeida OF, Wu Y.

J Alzheimers Dis. 2016;51(1):197-212. doi: 10.3233/JAD-150942.

PMID:
26836185
6.

NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.

Tamburri A, Dudilot A, Licea S, Bourgeois C, Boehm J.

PLoS One. 2013 Jun 4;8(6):e65350. doi: 10.1371/journal.pone.0065350. Print 2013.

7.

N-methyl-D-aspartate receptors are required for synaptic targeting of Alzheimer's toxic amyloid-β peptide oligomers.

Decker H, Jürgensen S, Adrover MF, Brito-Moreira J, Bomfim TR, Klein WL, Epstein AL, De Felice FG, Jerusalinsky D, Ferreira ST.

J Neurochem. 2010 Dec;115(6):1520-9. doi: 10.1111/j.1471-4159.2010.07058.x. Epub 2010 Nov 11.

8.

Local and Use-Dependent Effects of β-Amyloid Oligomers on NMDA Receptor Function Revealed by Optical Quantal Analysis.

Sinnen BL, Bowen AB, Gibson ES, Kennedy MJ.

J Neurosci. 2016 Nov 9;36(45):11532-11543.

9.

Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression.

Nabavi S, Kessels HW, Alfonso S, Aow J, Fox R, Malinow R.

Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):4027-32. doi: 10.1073/pnas.1219454110. Epub 2013 Feb 19.

10.

Neurotransmitter receptor and time dependence of the synaptic plasticity disrupting actions of Alzheimer's disease Aβ in vivo.

Klyubin I, Ondrejcak T, Hayes J, Cullen WK, Mably AJ, Walsh DM, Rowan MJ.

Philos Trans R Soc Lond B Biol Sci. 2013 Dec 2;369(1633):20130147. doi: 10.1098/rstb.2013.0147. Print 2014 Jan 5.

12.

Selective impairment of some forms of synaptic plasticity by oligomeric amyloid-β peptide in the mouse hippocampus: implication of extrasynaptic NMDA receptors.

Kervern M, Angeli A, Nicole O, Léveillé F, Parent B, Villette V, Buisson A, Dutar P.

J Alzheimers Dis. 2012;32(1):183-96.

PMID:
22785392
13.

Dysfunctional synapse in Alzheimer's disease - A focus on NMDA receptors.

Mota SI, Ferreira IL, Rego AC.

Neuropharmacology. 2014 Jan;76 Pt A:16-26. doi: 10.1016/j.neuropharm.2013.08.013. Epub 2013 Aug 22. Review.

PMID:
23973316
14.

Reciprocal disruption of neuronal signaling and Aβ production mediated by extrasynaptic NMDA receptors: a downward spiral.

Rush T, Buisson A.

Cell Tissue Res. 2014 May;356(2):279-86. doi: 10.1007/s00441-013-1789-1. Epub 2014 Feb 5. Review.

PMID:
24496511
15.

Turning off of GluN2B subunits and turning on of CICR in hippocampal LTD induction after developmental GluN2 subunit switch.

Yasuda H, Mukai H.

Hippocampus. 2015 Nov;25(11):1274-84. doi: 10.1002/hipo.22435. Epub 2015 Apr 18.

PMID:
25727316
16.

NMDA receptor regulation by amyloid-beta does not account for its inhibition of LTP in rat hippocampus.

Raymond CR, Ireland DR, Abraham WC.

Brain Res. 2003 Apr 11;968(2):263-72.

PMID:
12663096
17.

Aβ and NMDAR activation cause mitochondrial dysfunction involving ER calcium release.

Ferreira IL, Ferreiro E, Schmidt J, Cardoso JM, Pereira CM, Carvalho AL, Oliveira CR, Rego AC.

Neurobiol Aging. 2015 Feb;36(2):680-92. doi: 10.1016/j.neurobiolaging.2014.09.006. Epub 2014 Sep 6.

PMID:
25442114
18.

Ionotropic NMDA receptor signaling is required for the induction of long-term depression in the mouse hippocampal CA1 region.

Babiec WE, Guglietta R, Jami SA, Morishita W, Malenka RC, O'Dell TJ.

J Neurosci. 2014 Apr 9;34(15):5285-90. doi: 10.1523/JNEUROSCI.5419-13.2014.

19.

mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo.

Hu NW, Nicoll AJ, Zhang D, Mably AJ, O'Malley T, Purro SA, Terry C, Collinge J, Walsh DM, Rowan MJ.

Nat Commun. 2014 Mar 4;5:3374. doi: 10.1038/ncomms4374.

20.

Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways.

Roselli F, Hutzler P, Wegerich Y, Livrea P, Almeida OF.

PLoS One. 2009 Jun 23;4(6):e6011. doi: 10.1371/journal.pone.0006011.

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