ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013
GluN2B antagonism affects interneurons and leads to immediate and persistent changes in synaptic plasticity, oscillations, and behavior.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Metabotropic NMDAR Signaling Contributes to Sex Differences in Synaptic Plasticity and Episodic Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Therapeutic potential of N-methyl-D-aspartate receptor modulators in psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Loss of Grin2a causes a transient delay in the electrophysiological maturation of hippocampal parvalbumin interneurons.Communications biology · 2023Article
- [Advances on GABAergic interneurons in autism spectrum disorders].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Quantitative Analysis of Retinal Structure and Function in Two Chromosomally Altered Mouse Models of Down Syndrome.Investigative ophthalmology & visual science · 2020Article
- Hippocampal µ-opioid receptors on GABAergic neurons mediate stress-induced impairment of memory retrieval.Molecular psychiatry · 2020Article
- Insoluble Aβ overexpression in anDisease models & mechanisms · 2019Article
- Article
- Phosphoproteomic Alterations of Ionotropic Glutamate Receptors in the Hippocampus of the Ts65Dn Mouse Model of Down Syndrome.Frontiers in molecular neuroscience · 2018Article
- Rodent models in Down syndrome research: impact and future opportunities.Disease models & mechanisms · 2017Review
- Reduced ethanol drinking following selective cortical interneuron deletion of the GluN2B NMDA receptors subunit.Alcohol (Fayetteville, N.Y.) · 2017Article
- The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome.Frontiers in cellular neuroscience · 2017Review
- Decrease of SYNGAP1 in GABAergic cells impairs inhibitory synapse connectivity, synaptic inhibition and cognitive function.Nature communications · 2016Article
- Negative Allosteric Modulators Selective for The NR2B Subtype of The NMDA Receptor Impair Cognition in Multiple Domains.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Ketamine and phencyclidine: the good, the bad and the unexpected.British journal of pharmacology · 2015Review
- Article
- Altered GluN2B NMDA receptor function and synaptic plasticity during early pathology in the PS2APP mouse model of Alzheimer's disease.Neurobiology of disease · 2015Article
- Timing of therapies for Down syndrome: the sooner, the better.Frontiers in behavioral neuroscience · 2015Review
- Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.Drug design, development and therapy · 2015Review
- Specific Roles of NMDA Receptor Subunits in Mental Disorders.Current molecular medicine · 2015Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although antagonists to GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) have been widely considered to be neuroprotective under certain pathological conditions, their immediate and lasting impacts on synaptic, circuit, and cognitive functions are poorly understood. In hippocampal slices, we found that the GluN2B-selective antagonist Ro25-6981 (Ro25) reduced synaptic NMDAR responses and consequently neuronal output in a subpopulation of GABAergic interneurons, but not pyramidal neurons. Consistent with these effects, Ro25 reduced GABAergic responses in pyramidal neurons and hence could affect circuit functions by altering the excitation/inhibition balance in the brain. In slices from Ts65Dn mice, a Down syndrome model with excess inhibition and cognitive impairment, acutely applied Ro25-rescued long-term potentiation (LTP) and gamma oscillation deficits, whereas prolonged dosing induced persistent rescue of LTP. In contrast, Ro25 did not impact LTP in wild-type (wt) mice but reduced gamma oscillations both acutely and following prolonged treatment. Although acute Ro25 treatment impaired memory performance in wt mice, memory deficits in Ts65Dn mice were unchanged. Thus, GluN2B-NMDARs contribute to the excitation/inhibition balance via impacts on interneurons, and blocking GluN2B-NMDARs can alter functions that depend on this balance, including synaptic plasticity, gamma oscillations, and memory. That prolonged GluN2B antagonism leads to persistent changes in synaptic and circuit functions, and that the influence of GluN2B antagonism differs between wt and disease model mice, provide critical insight into the therapeutic potential and possible liabilities of GluN2B antagonists.
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