ArticleJournal of computational neuroscience2016
A biophysical model of the cortex-basal ganglia-thalamus network in the 6-OHDA lesioned rat model of Parkinson's disease.
Article in Journal of computational neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 111 citations in OpenAlex.
- In silico model of basal ganglia deep brain stimulation in Parkinson's disease captures range of effective parameters for pathological beta power suppression.PLoS computational biology · 2026Article
- Effect of frequency on dual target deep brain stimulation.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2026Article
- A Hybrid ODE-NN Framework for Modeling Incomplete Physiological Systems.IEEE transactions on bio-medical engineering · 2025Article
- Break-up and recovery of harmony between direct and indirect pathways in the basal ganglia: Huntington's disease and treatment.Cognitive neurodynamics · 2024Article
- Quantifying harmony between direct and indirect pathways in the basal ganglia: healthy and Parkinsonian states.Cognitive neurodynamics · 2024Article
- Refining Brain Stimulation Therapies: An Active Learning Approach to Personalization.Research square · 2024Article
- Refining Brain Stimulation Therapies: An Active Learning Approach to Personalization.bioRxiv : the preprint server for biology · 2024Article
- Mathematical derivation and mechanism analysis of beta oscillations in a cortex-pallidum model.Cognitive neurodynamics · 2024Article
- Closed-loop modulation of model parkinsonian beta oscillations based on CAR-fuzzy control algorithm.Cognitive neurodynamics · 2023Article
- Improved control effect of pathological oscillations by using delayed feedback stimulation in neural mass model with pedunculopontine nucleus.Brain and behavior · 2023Article
- The Therapeutic Frequency Profile of Subthalamic Nucleus Deep Brain Stimulation in Rats Is Shaped by Antidromic Spike Failure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Monitoring time domain characteristics of Parkinson's disease using 3D memristive neuromorphic system.Frontiers in computational neuroscience · 2023Article
- Synaptic network structure shapes cortically evoked spatio-temporal responses of STN and GPe neurons in a computational model.Frontiers in neuroinformatics · 2023Article
- Model-based optogenetic stimulation to regulate beta oscillations in Parkinsonian neural networks.Cognitive neurodynamics · 2022Article
- Excitatory deep brain stimulation quenches beta oscillations arising in a computational model of the subthalamo-pallidal loop.Scientific reports · 2022Article
- Deep brain stimulation in the subthalamic nucleus for Parkinson's disease can restore dynamics of striatal networks.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neurorobotic Models of Neurological Disorders: A Mini Review.Frontiers in neurorobotics · 2021Review
- Adaptive Parameter Modulation of Deep Brain Stimulation Based on Improved Supervisory Algorithm.Frontiers in neuroscience · 2021Article
- Neuro4PD: An Initial Neurorobotics Model of Parkinson's Disease.Frontiers in neurorobotics · 2021Article
- Endocannabinoids and Dopamine Balance Basal Ganglia Output.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Electrical stimulation of sub-cortical brain regions (the basal ganglia), known as deep brain stimulation (DBS), is an effective treatment for Parkinson's disease (PD). Chronic high frequency (HF) DBS in the subthalamic nucleus (STN) or globus pallidus interna (GPi) reduces motor symptoms including bradykinesia and tremor in patients with PD, but the therapeutic mechanisms of DBS are not fully understood. We developed a biophysical network model comprising of the closed loop cortical-basal ganglia-thalamus circuit representing the healthy and parkinsonian rat brain. The network properties of the model were validated by comparing responses evoked in basal ganglia (BG) nuclei by cortical (CTX) stimulation to published experimental results. A key emergent property of the model was generation of low-frequency network oscillations. Consistent with their putative pathological role, low-frequency oscillations in model BG neurons were exaggerated in the parkinsonian state compared to the healthy condition. We used the model to quantify the effectiveness of STN DBS at different frequencies in suppressing low-frequency oscillatory activity in GPi. Frequencies less than 40 Hz were ineffective, low-frequency oscillatory power decreased gradually for frequencies between 50 Hz and 130 Hz, and saturated at frequencies higher than 150 Hz. HF STN DBS suppressed pathological oscillations in GPe/GPi both by exciting and inhibiting the firing in GPe/GPi neurons, and the number of GPe/GPi neurons influenced was greater for HF stimulation than low-frequency stimulation. Similar to the frequency dependent suppression of pathological oscillations, STN DBS also normalized the abnormal GPi spiking activity evoked by CTX stimulation in a frequency dependent fashion with HF being the most effective. Therefore, therapeutic HF STN DBS effectively suppresses pathological activity by influencing the activity of a greater proportion of neurons in the output nucleus of the BG.
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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.