ArticleBiological psychiatry2018
Presynaptic Effects of N-Methyl-D-Aspartate Receptors Enhance Parvalbumin Cell-Mediated Inhibition of Pyramidal Cells in Mouse Prefrontal Cortex.
Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Bidirectional control of vesicular GABA release, LTP, and amotivation by GluN2D-selective allosteric modulators and ketamine.Cell reports · 2026Article
- Schizophrenia Pathophysiology: Neurotransmitter Dysfunctions and Biomarker Frontiers.Current topics in medicinal chemistry · 2026Review
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 2025Review
- Article
- Gamma Oscillations as a Biomarker of Neural Circuit Function in Psychosis: Where Are We, and Where Do We Go from Here?Advances in neurobiology · 2024Review
- Treatment resistance NMDA receptor pathway polygenic score is associated with brain glutamate in schizophrenia.Schizophrenia research · 2023Article
- Pathway-specific contribution of parvalbumin interneuron NMDARs to synaptic currents and thalamocortical feedforward inhibition.Molecular psychiatry · 2022Article
- Synaptic Variability and Cortical Gamma Oscillation Power in Schizophrenia.The American journal of psychiatry · 2022Article
- Modulation of GABAergic Synaptic Transmission by NMDA Receptors in the Dorsal Horn of the Spinal Cord.Frontiers in molecular neuroscience · 2022Article
- Targeting prefrontal cortex GABAergic microcircuits for the treatment of alcohol use disorder.Frontiers in synaptic neuroscience · 2022Review
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Network Asynchrony Underlying Increased Broadband Gamma Power.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Interneuron NMDA Receptor Ablation Induces Hippocampus-Prefrontal Cortex Functional Hypoconnectivity after Adolescence in a Mouse Model of Schizophrenia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?Frontiers in psychiatry · 2019Review
- Input-specific maturation of NMDAR-mediated transmission onto parvalbumin-expressing interneurons in layers 2/3 of the visual cortex.Journal of neurophysiology · 2018Article
- Acute ketamine dysregulates task-related gamma-band oscillations in thalamo-cortical circuits in schizophrenia.Brain : a journal of neurology · 2018Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTesting hypotheses regarding the role of N-methyl-D-aspartate receptor (NMDAR) hypofunction in schizophrenia requires understanding the mechanisms of NMDAR regulation of prefrontal cortex (PFC) circuit function. NMDAR antagonists are thought to produce pyramidal cell (PC) disinhibition. However, inhibitory parvalbumin-positive basket cells (PVBCs) have modest NMDAR-mediated excitatory drive and thus are unlikely to participate in NMDAR antagonist-mediated disinhibition. Interestingly, recent studies demonstrated that presynaptic NMDARs enhance transmitter release at central synapses. Thus, if presynaptic NMDARs enhance gamma-aminobutyric acid release at PVBC-to-PC synapses, they could participate in NMDAR-dependent PC disinhibition. Here, we examined whether presynaptic NMDAR effects could modulate gamma-aminobutyric acid release at PVBC-to-PC synapses in mouse PFC.
methodsUsing whole-cell recordings from synaptically connected pairs in mouse PFC, we determined whether NMDA or NMDAR antagonist application affects PVBC-to-PC inhibition in a manner consistent with a presynaptic mechanism.
resultsNMDAR activation enhanced by ∼40% the synaptic current at PVBC-to-PC pairs. This effect was consistent with a presynaptic mechanism given that it was 1) observed with postsynaptic NMDARs blocked by intracellular MK801, 2) associated with a lower rate of transmission failures and a higher transmitter release probability, and 3) blocked by intracellular MK801 in the PVBC. NMDAR antagonist application did not affect the synaptic currents in PVBC-to-PC pairs, but it reduced the inhibitory currents elicited in PCs with simultaneous glutamate release by extracellular stimulation.
conclusionsWe demonstrate that NMDAR activation enhances PVBC-to-PC inhibition in a manner consistent with presynaptic mechanisms, and we suggest that the functional impact of this presynaptic effect depends on the activity state of the PFC network.
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