ArticlePsychopharmacology2014
Aberrant glutamate signaling in the prefrontal cortex and striatum of the spontaneously hypertensive rat model of attention-deficit/hyperactivity disorder.
Article in Psychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Attention-deficit/hyperactivity disorder in children with a history of febrile seizures: a systematic review and meta-analysis.European journal of pediatrics · 2025Pooled it
- A comprehensive overview of the biological foundations of ADHD.Bioscience reports · 2026Review
- Aniracetam restores the excitation-inhibition balance of neurotransmitters in the prefrontal cortex of mice with ADHD.Scientific reports · 2026Article
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Transcriptomic Dysregulation in Animal Models of Attention-Deficit Hyperactivity Disorder and Nicotine Dependence Suggests Shared Neural Mechanisms.Brain and behavior · 2025Article
- Aniracetam Ameliorates Attention Deficit Hyperactivity Disorder Behavior in Adolescent Mice.eNeuro · 2025Article
- Aberrant glutamatergic systems underlying impulsive behaviors: Insights from clinical and preclinical research.Progress in neuro-psychopharmacology & biological psychiatry · 2024Review
- Learning and Memory Impairments With Attention-Deficit/Hyperactivity Disorder.Physiological research · 2024Review
- Role of Glutamate Receptor-related Biomarkers in the Etiopathogenesis of ADHD.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024Article
- Parvalbumin interneuron deficiency in the prefrontal and motor cortices of spontaneously hypertensive rats: an attention-deficit hyperactivity disorder animal model insight.Frontiers in psychiatry · 2024Article
- Glutamate receptor genetic variants affected peripheral glutamatergic transmission and treatment induced improvement of Indian ADHD probands.Scientific reports · 2023Article
- Profiling transcriptomic responses of human stem cell-derived medium spiny neuron-like cells to exogenous phasic and tonic neurotransmitters.Molecular and cellular neurosciences · 2023Article
- Kainate receptor subunit 1 (GRIK1) risk variants and GRIK1 deficiency were detected in the Indian ADHD probands.Scientific reports · 2022Article
- Deficiency of transmembrane AMPA receptor regulatory protein γ-8 leads to attention-deficit hyperactivity disorder-like behavior in mice.Zoological research · 2022Article
- The electroretinogram b-wave amplitude: a differential physiological measure for Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorder.Journal of neurodevelopmental disorders · 2022Article
- An atlas of transcriptionally defined cell populations in the rat ventral tegmental area.Cell reports · 2022Article
- Increased Serum Level of CCL5 in Children with Attention‑Deficit/Hyperactivity Disorder: First Results about Serum Chemokines.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022Article
- Chronic Administrations of Guanfacine on Mesocortical Catecholaminergic and Thalamocortical Glutamatergic Transmissions.International journal of molecular sciences · 2021Article
- Neuroinflammation as a risk factor for attention deficit hyperactivity disorder.Pharmacology, biochemistry, and behavior · 2019Review
- Chronic Methylphenidate Alters Tonic and Phasic Glutamate Signaling in the Frontal Cortex of a Freely-Moving Rat Model of ADHD.Neurochemical research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleAttention-deficit/hyperactivity disorder (ADHD) is thought to involve hypofunctional catecholamine systems in the striatum, nucleus accumbens, and prefrontal cortex (PFC); however, recent clinical evidence has implicated glutamate dysfunction in the pathophysiology of ADHD. Recent studies show that increased stimulation of dopamine D2 and D4 receptors causes inhibition of N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, respectively. The spontaneously hypertensive rat (SHR) model of ADHD combined type (C) has been found to have a hypofunctional dopamine system in the ventral striatum, nucleus accumbens, and PFC compared to the control Wistar Kyoto (WKY) strain.
objectivesBased on the current understanding of typical dopamine-glutamate interactions, we hypothesized that the SHR model of ADHD would have a hyperfunctional glutamate system terminating in the striatum, nucleus accumbens, and PFC.
resultsHigh-speed amperometric recordings combined with four-channel microelectrode arrays to directly measure glutamate dynamics showed increased evoked glutamate release in the PFC (cingulate and infralimbic cortices, p < 0.05) and also in the striatum (p < 0.05) of the SHR (ADHD-C) as compared to the WKY. Finally, glutamate uptake was discovered to be aberrant in the PFC, but not the striatum, of the SHR when compared to the control WKY strain.
conclusionsThese results suggest that the glutamatergic system in the PFC of the SHR model of ADHD is hyperfunctional and that targeting glutamate in the PFC could lead to the development of novel therapeutics for the treatment of ADHD.
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