ArticleBritish journal of pharmacology2014
Allosteric modulation of GluN2C/GluN2D-containing NMDA receptors bidirectionally modulates dopamine release: implication for Parkinson's disease.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- GluN2D NMDA Receptors: Bridging Physiology and Pathology.Biological psychiatry · 2026Review
- GluN2C/D-containing NMDA receptors enhance temporal summation and increase sound-evoked and spontaneous firing in the inferior colliculus.The Journal of physiology · 2025Article
- Knocking Out TAAR5: A Pathway to Enhanced Neurogenesis and Dopamine Signaling in the Striatum.Cells · 2024Article
- 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
- Aberrant somatic calcium channel function in cNurr1 and LRRK2-G2019S mice.NPJ Parkinson's disease · 2023Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Deficits in Motor Performance, Neurotransmitters and Synaptic Plasticity in Elderly and Experimental Parkinsonian Mice Lacking GPR37.Frontiers in aging neuroscience · 2020Article
- The origin of NMDA receptor hypofunction in schizophrenia.Pharmacology & therapeutics · 2020Review
- Ketamine and its metabolite (2R,6R)-hydroxynorketamine induce lasting alterations in glutamatergic synaptic plasticity in the mesolimbic circuit.Molecular psychiatry · 2018Article
- NMDA receptor blockade ameliorates abnormalities of spike firing of subthalamic nucleus neurons in a parkinsonian nonhuman primate.Journal of neuroscience research · 2018Article
- A Novel Negative Allosteric Modulator Selective for GluN2C/2D-Containing NMDA Receptors Inhibits Synaptic Transmission in Hippocampal Interneurons.ACS chemical neuroscience · 2018Article
- 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
- Striatal Tyrosine Hydroxylase Is Stimulated via TAAR1 by 3-Iodothyronamine, But Not by Tyramine or β-Phenylethylamine.Frontiers in pharmacology · 2018Article
- NMDA Receptors in the Central Nervous System.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Enhancing NMDA Receptor Function: Recent Progress on Allosteric Modulators.Neural plasticity · 2017Review
- NMDA Receptors Containing the GluN2D Subunit Control Neuronal Function in the Subthalamic Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Potentiation of NMDA receptor-mediated transmission in striatal cholinergic interneurons.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAllosteric modulators of ionotropic receptors and GPCRs might constitute valuable therapeutic tools for intervention in several diseases, including Parkinson's disease (PD). However, the possibility that some of these compounds could alter neurotransmission in health and disease has not been thoroughly examined. Hence, we determined whether CIQ, a positive allosteric modulator of NMDA receptors that contain the GluN2C or GluN2D subunits, modulates dopamine release in the striatum of control mice and of a mouse model of presymptomatic Parkinsonism. EXPERIMENTAL APPROACH: We used amperometry to measure, in mouse brain slices containing the dorsal striatum, dopamine release evoked by stimulations that mimicked tonic (single pulses) or phasic (trains) activity. We used control mice and mice with a partial, 6-hydroxydopamine-induced, degeneration of dopaminergic neurons in the substantia nigra. KEY
resultsIn control mice, CIQ inhibited tonic dopamine release and induced an initial inhibition followed by a long-lasting increase in phasic release. Pirenzepine, a muscarinic receptor antagonist, blocked the depression of release induced by CIQ, but not the long-lasting potentiation. CIQ also increased action potential firing in striatal cholinergic interneurons. In the partially dopamine-depleted striatum, CIQ induced an inhibition followed by a potentiation of both tonic and phasic release, but did not significantly increase the firing of cholinergic interneurons. CONCLUSIONS AND IMPLICATIONS: CIQ has bidirectional, activity- and ACh-dependent, modulatory effects on dopamine release in the striatum. This study suggests a potentially valuable means to enhance dopamine release in presymptomatic Parkinsonism.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.