ArticleFrontiers in neural circuits2019
A Computational Model of Loss of Dopaminergic Cells in Parkinson's Disease Due to Glutamate-Induced Excitotoxicity.
Article in Frontiers in neural circuits, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 44 citations in OpenAlex.
- Environmental Factors Drive Neurodegenerative Diseases Through Glutamate Excitotoxicity: A Convergent Mechanistic Pathway.Neuroscience bulletin · 2026Review
- Therapeutic Potential of Sea Cucumber-Derived Bioactives in the Prevention and Management of Brain-Related Disorders: A Comprehensive Review.Marine drugs · 2025Review
- Synergistic Reinforcement Learning by Cooperation of the Cerebellum and Basal Ganglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Multiple time delay induced Hopf bifurcation of a cortex - basal ganglia model for Parkinson's Disease.Cognitive neurodynamics · 2024Article
- Parkinson's Disease Risk and Hyperhomocysteinemia: The Possible Link.Cellular and molecular neurobiology · 2023Review
- Cannabidiol Reduces Short- and Long-Term High Glutamate Release after Severe Traumatic Brain Injury and Improves Functional Recovery.Pharmaceutics · 2022Article
- Plasticity impairment alters community structure but permits successful pattern separation in a hippocampal network model.Frontiers in cellular neuroscience · 2022Article
- The neuroprotective effects of fisetin, a natural flavonoid in neurodegenerative diseases: Focus on the role of oxidative stress.Frontiers in pharmacology · 2022Review
- A Multi-Scale Computational Model of Levodopa-Induced Toxicity in Parkinson's Disease.Frontiers in neuroscience · 2022Article
- DOPA Homeostasis by Dopamine: A Control-Theoretic View.International journal of molecular sciences · 2021Article
- The theoretical mechanism of Parkinson's oscillation frequency bands: a computational model study.Cognitive neurodynamics · 2021Article
- Influence of energy deficiency on the subcellular processes of Substantia Nigra Pars Compacta cell for understanding Parkinsonian neurodegeneration.Scientific reports · 2021Article
- A Multiscale, Systems-Level, Neuropharmacological Model of Cortico-Basal Ganglia System for Arm Reaching Under Normal, Parkinsonian, and Levodopa Medication Conditions.Frontiers in computational neuroscience · 2021Article
- Neuro4PD: An Initial Neurorobotics Model of Parkinson's Disease.Frontiers in neurorobotics · 2021Article
- Modeling NeurodegenerationFrontiers in neuroinformatics · 2021Article
- The environmental toxicant ziram enhances neurotransmitter release and increases neuronal excitability via the EAG family of potassium channels.Neurobiology of disease · 2020Article
- Article
- A Multi-Scale Computational Model of Excitotoxic Loss of Dopaminergic Cells in Parkinson's Disease.Frontiers in neuroinformatics · 2020Article
- Neurodegenerative Diseases - Is Metabolic Deficiency the Root Cause?Frontiers in neuroscience · 2020Review
- A Computational Model of Loss of Dopaminergic Cells in Parkinson's Disease Due to Glutamate-Induced Excitotoxicity.Frontiers in neural circuits · 2019Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurodegenerative disease associated with progressive and inexorable loss of dopaminergic cells in Substantia Nigra pars compacta (SNc). Although many mechanisms have been suggested, a decisive root cause of this cell loss is unknown. A couple of the proposed mechanisms, however, show potential for the development of a novel line of PD therapeutics. One of these mechanisms is the peculiar metabolic vulnerability of SNc cells compared to other dopaminergic clusters; the other is the SubThalamic Nucleus (STN)-induced excitotoxicity in SNc. To investigate the latter hypothesis computationally, we developed a spiking neuron network-model of SNc-STN-GPe system. In the model, prolonged stimulation of SNc cells by an overactive STN leads to an increase in 'stress' variable; when the stress in a SNc neuron exceeds a stress threshold, the neuron dies. The model shows that the interaction between SNc and STN involves a positive-feedback due to which, an initial loss of SNc cells that crosses a threshold causes a runaway-effect, leading to an inexorable loss of SNc cells, strongly resembling the process of neurodegeneration. The model further suggests a link between the two aforementioned mechanisms of SNc cell loss. Our simulation results show that the excitotoxic cause of SNc cell loss might initiate by weak-excitotoxicity mediated by energy deficit, followed by strong-excitotoxicity, mediated by a disinhibited STN. A variety of conventional therapies were simulated to test their efficacy in slowing down SNc cell loss. Among them, glutamate inhibition, dopamine restoration, subthalamotomy and deep brain stimulation showed superior neuroprotective-effects in the proposed model.
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