ArticleProceedings of the National Academy of Sciences of the United States of America2001
Glutamatergic modulation of hyperactivity in mice lacking the dopamine transporter.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 168 citations in OpenAlex.
- A comprehensive overview of the biological foundations of ADHD.Bioscience reports · 2026Review
- Hippocampal transcriptome profiling in a 22q11.2 deletion syndrome mouse model: comparison with human schizophrenia.Molecular brain · 2026Article
- Delta Opioid Receptors within the Cortico-Thalamic Circuitry Underlie Hyperactivity Induced by High-Dose Morphine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Enhancing Hydroxyl Metabolite Analysis through In Situ Derivatization-Enabled Desorption Electrospray Ionization-Mass Spectrometry.Analytical chemistry · 2025Article
- Revisiting the Role of Serotonin in Attention-Deficit Hyperactivity Disorder: New Insights from Preclinical and Clinical Studies.Clinical drug investigation · 2025Review
- Article
- The Ins and Outs of Dopamine Transporter Gene Manipulation: In Vivo Models of DAT Dysfunction.Advances in neurobiology · 2025Review
- An updated review on animal models to study attention-deficit hyperactivity disorder.Translational psychiatry · 2024Review
- Preclinical Pharmacology of CX1837, a High-Impact Ampakine with an Improved Safety Margin: Implications for Treating Alzheimer's Disease and Ischemic Stroke.Current Alzheimer research · 2024Article
- Shifts in naturalistic behaviors induced by early social isolation stress are associated with adult binge-like eating in female rats.Frontiers in behavioral neuroscience · 2024Article
- Chronic Methylphenidate Effects on Brain Gene Expression: An Exploratory Review.Psychology research and behavior management · 2024Review
- Increasing dopamine synthesis in nigrostriatal circuits increases phasic dopamine release and alters dorsal striatal connectivity: implications for schizophrenia.Schizophrenia (Heidelberg, Germany) · 2023Article
- Dopamine Transporter Deficient Rodents: Perspectives and Limitations for Neuroscience.Biomolecules · 2023Review
- Haloperidol-Induced Immediate Early Genes in Striatopallidal Neurons Requires the Converging Action of cAMP/PKA/DARPP-32 and mTOR Pathways.International journal of molecular sciences · 2022Article
- Spironolactone alleviates schizophrenia-related reversal learning in Tcf4 transgenic mice subjected to social defeat.Schizophrenia (Heidelberg, Germany) · 2022Article
- Blood Glutamate Scavenging With Pyruvate as a Novel Preventative and Therapeutic Approach for Depressive-Like Behavior Following Traumatic Brain Injury in a Rat Model.Frontiers in neuroscience · 2022Article
- Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model.Genes, brain, and behavior · 2022Article
- Responsivity of the Striatal Dopamine System to Methylphenidate-A Within-Subject I-123-β-CIT-SPECT Study in Male Children and Adolescents With Attention-Deficit/Hyperactivity Disorder.Frontiers in psychiatry · 2022Article
- Review of rodent models of attention deficit hyperactivity disorder.Neuroscience and biobehavioral reviews · 2022Review
- Early Adolescence Prefrontal Cortex Alterations in Female Rats Lacking Dopamine Transporter.Biomedicines · 2021Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In the brain, dopamine exerts an important modulatory influence over behaviors such as emotion, cognition, and affect as well as mechanisms of reward and the control of locomotion. The dopamine transporter (DAT), which reuptakes the released neurotransmitter into presynaptic terminals, is a major determinant of the intensity and duration of the dopaminergic signal. Knockout mice lacking the dopamine transporter (DAT-KO mice) display marked changes in dopamine homeostasis that result in elevated dopaminergic tone and pronounced locomotor hyperactivity. A feature of DAT-KO mice is that their hyperactivity can be inhibited by psychostimulants and serotonergic drugs. The pharmacological effect of these drugs occurs without any observable changes in dopaminergic parameters, suggesting that other neurotransmitter systems in addition to dopamine might contribute to the control of locomotion in these mice. We report here that the hyperactivity of DAT-KO mice can be markedly further enhanced when N-methyl-d-aspartate receptor-mediated glutamatergic transmission is blocked. Conversely, drugs that enhance glutamatergic transmission, such as positive modulators of l-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate glutamate receptors, suppress the hyperactivity of DAT-KO mice. Interestingly, blockade of N- methyl-d-aspartate receptors prevented the inhibitory effects of both psychostimulant and serotonergic drugs on hyperactivity. These findings support the concept of a reciprocal functional interaction between dopamine and glutamate in the basal ganglia and suggest that agents modulating glutamatergic transmission may represent an approach to manage conditions associated with dopaminergic dysfunction.
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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.