ArticleMetabolic brain disease2013
The preventive effect of NR2B and NR2D-containing NMDAR antagonists on Aβ-induced LTP disruption in the dentate gyrus of rats.
Article in Metabolic brain disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Extracellular Vesicles from Peripheral Blood Mononuclear Cells of Hyperammonemic Rats Induce Neuroinflammation in Hippocampus, Impairing Memory and Learning in Normal Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Extrasynaptic NMDA receptors in acute and chronic excitotoxicity: implications for preventive treatments of ischemic stroke and late-onset Alzheimer's disease.Molecular neurodegeneration · 2023Review
- Expression Changes of NMDA and AMPA Receptor Subunits in the Hippocampus in rats with Diabetes Induced by Streptozotocin Coupled with Memory Impairment.Neurochemical research · 2019Article
- Xuefu zhuyu decoction improves cognitive impairment in experimental traumatic brain injury via synaptic regulation.Oncotarget · 2017Article
- Abeta(1-42) enhances neuronal excitability in the CA1 via NR2B subunit-containing NMDA receptors.Neural plasticity · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid β-protein (Aβ) in the brain of Alzheimer's disease (AD) potently inhibits the synaptic plasticity subsequently causing the cognitive deficits. Long-term potentiation (LTP) of synaptic transmission is thought to be an important cellular mechanism underlying memory formation. Different NR2 subunits are involved in NMDA receptor-dependent LTP. In the present study, we investigated the roles of NR2B and NR2D-containing NMDAR on Aβ(1-42)-induced LTP deficits in the hippocampal slices of rats by using selective NMDAR antagonists. First, we found that Aβ(1-42) significantly inhibited the LTP in the dentate gyrus of slices as reported before. Following that the Aβ(1-42)-induced LTP inhibition was prevented by the pre-perfusion of the specific NR2B-containing NMDAR antagonists ifenprodil (approximately >200-fold selectivity for NR2B) and Ro25-6981 (>3,000-fold selectivity for NR2B), as well as PPDA, a specific NR2D receptor antagonist. Meanwhile, the antagonists on their own had no or only partial effects on the normal LTP in the same dose condition. These findings not only support the effects of NR2B and NR2D subunits on Aβ(1-42)-induced LTP deficits, but also imply that preferentially targeting NR2B- and NR2D-containing NMDARs may provide an effective means to prevent cognitive deficits in the early AD.
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