ArticleCNS neuroscience & therapeutics2018
CIQ, a positive allosteric modulator of GluN2C/D-containing N-methyl-d-aspartate receptors, rescues striatal synaptic plasticity deficit in a mouse model of Parkinson's disease.
Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 16 citations in OpenAlex.
- GluN2C/D-containing NMDA receptors enhance temporal summation and increase sound-evoked and spontaneous firing in the inferior colliculus.The Journal of physiology · 2025Article
- Selective enhancement of the interneuron network and gamma-band power via GluN2C/GluN2D NMDA receptor potentiation.The Journal of physiology · 2025Article
- Activation of GluN2D-containing NMDA receptors promotes development of axons and axon-carrying dendrites of cortical interneurons.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- GluN2C/D-containing NMDA receptors enhance temporal summation and increase sound-evoked and spontaneous firing in the inferior colliculus.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic potential of N-methyl-D-aspartate receptor modulators in psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Differential regulation of STP, LTP and LTD by structurally diverse NMDA receptor subunit-specific positive allosteric modulators.Neuropharmacology · 2022Article
- Transcriptome profiling of five brain regions in a 6-hydroxydopamine rat model of Parkinson's disease.CNS neuroscience & therapeutics · 2021Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Building a Bridge Between NMDAR-Mediated Excitotoxicity and Mitochondrial Dysfunction in Chronic and Acute Diseases.Cellular and molecular neurobiology · 2021Review
- NMDA GluN2C/2D receptors contribute to synaptic regulation and plasticity in the anterior cingulate cortex of adult mice.Molecular brain · 2021Article
- Discovery of Dihydropyrrolo[1,2-Journal of medicinal chemistry · 2020Article
- CIQ, a positive allosteric modulator of GluN2C/D-containing N-methyl-d-aspartate receptors, rescues striatal synaptic plasticity deficit in a mouse model of Parkinson's disease.CNS neuroscience & therapeutics · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo investigate if CIQ, a positive allosteric modulator of N-methyl-d-aspartate receptors (NMDARs) containing GluN2C/D subunits, rescues the loss of long-term potentiation (LTP) and forelimb-use asymmetry in a mouse model of Parkinson's disease (PD).
methodsWe have used electrophysiology in brain slices and the cylinder test to examine the effect of CIQ on glutamatergic synaptic transmission, synaptic plasticity, and forelimb-use in the unilateral 6-hydroxydopamine-lesion mouse model of PD.
resultsCIQ, applied in the perfusion solution, reversibly reduced glutamatergic synaptic transmission in the dopamine-depleted striatum and had no effect in the dopamine-intact striatum. LTP, a dopamine- and NMDAR-dependent form of synaptic plasticity, was induced in the dopamine-intact striatum but was lost in the dopamine-depleted striatum. This impaired LTP was restored in the presence of CIQ applied in the perfusion solution. This treatment, however, prevented LTP induction in control slices. In brain slices from mice which received single and chronic intraperitoneal injections of CIQ, LTP was restored in the dopamine-depleted striatum and unaffected in the dopamine-intact striatum. Forelimb-use asymmetry, a test which assesses deficits in paw usage in the unilateral lesion model of PD, was reversed by systemic chronic treatment with CIQ.
conclusionA positive allosteric modulator of GluN2C/D-containing NMDARs rescues LTP and forelimb-use asymmetry in a mouse model of PD. This study proposes GluN2D as a potential candidate for therapeutic intervention in PD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.