2011
DOI: 10.1016/j.neurobiolaging.2010.01.011
|View full text |Cite
|
Sign up to set email alerts
|

Early neuronal dysfunction by amyloid β oligomers depends on activation of NR2B-containing NMDA receptors

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

13
204
6
1

Year Published

2012
2012
2020
2020

Publication Types

Select...
8

Relationship

2
6

Authors

Journals

citations
Cited by 226 publications
(224 citation statements)
references
References 37 publications
13
204
6
1
Order By: Relevance
“…GluN2B antagonist, prevented LTP impairment, baseline synaptic transmission reduction, neuronal spontaneous network activity decrease and retraction of synaptic contacts induced by Aβ oligomers (Ronicke et al, 2011). Moreover, in rats co-injected with Aβ and ifenprodil prevented Aβ-mediated inhibition of plasticity (Hu et al, 2009).…”
Section: A C C E P T E D Accepted Manuscriptmentioning
confidence: 91%
“…GluN2B antagonist, prevented LTP impairment, baseline synaptic transmission reduction, neuronal spontaneous network activity decrease and retraction of synaptic contacts induced by Aβ oligomers (Ronicke et al, 2011). Moreover, in rats co-injected with Aβ and ifenprodil prevented Aβ-mediated inhibition of plasticity (Hu et al, 2009).…”
Section: A C C E P T E D Accepted Manuscriptmentioning
confidence: 91%
“…Lyophilized A␤(1-42),5-TMR (AnaSpec) that had been resuspended in 1,1,1,3,3,3-hexafluoro-2-propanol were used to prepare oA␤ 1-42 -TMR by diluting 5 mM A␤(1-42),5-TMR in Me 2 SO to a concentration of 100 M in HEPES buffer, pH 7.4. The solution was immediately vortexed and sonicated for 2 min and then incubated at 4°C for 24 h (Stine et al, 2003;Catalano et al, 2006;Rönicke et al, 2011). The scrambled A␤ 1-42 (catalog #25382; AnaSpec) was labeled by incubating the peptide with TMR (6-carboxytetramethylrhodamine, succinimidyl-ester; Invitrogen) in HEPES buffer, pH 7.4, for 24 h in 4°C at a 1:2 ratio.…”
Section: Methodsmentioning
confidence: 99%
“…Recent evidence has suggested that oA␤ impairs synaptic plasticity and causes cognitive failure in AD before plaque deposition and neuronal cell death (Walsh and Selkoe, 2007;Rönicke et al, 2011). oA␤-mediated spine loss, disruption of synaptic plasticity, and subsequent abnormalities in spine morphology could be mediated by action potentials, nAChRs, NMDA receptors, or AMPA receptors (Wei et al, 2010).…”
Section: Possible Mechanism Of Transmissionmentioning
confidence: 99%
See 1 more Smart Citation
“…In particular, the protein synthesis-dependent late phase of LTP (L-LTP) is impaired in the hippocampus of various AD transgenic mouse models and in Aβ-treated hippocampal slices (4,9), whereas LTD is facilitated (10) or not altered (10)(11)(12). It has been reported recently that Aβ-induced inhibition of LTP is mediated by extrasynaptic NMDA receptor activity, which prevents phosphorylation of the transcription factor cAMP response element-binding protein (13,14).…”
mentioning
confidence: 99%