ArticleFrontiers in neural circuits2015
Subthalamic deep brain stimulation reduces pathological information transmission to the thalamus in a rat model of parkinsonism.
Article in Frontiers in neural circuits, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Systematic review of rodent studies of deep brain stimulation for the treatment of neurological, developmental and neuropsychiatric disorders.Translational psychiatry · 2024Pooled it
- Cellular, molecular, and clinical mechanisms of action of deep brain stimulation-a systematic review on established indications and outlook on future developments.EMBO molecular medicine · 2019Pooled it
- Pallidal deep brain stimulation modulates excessive cortical high β phase amplitude coupling in Parkinson disease.Brain stimulationTrial
- Article
- Review
- Excitatory deep brain stimulation quenches beta oscillations arising in a computational model of the subthalamo-pallidal loop.Scientific reports · 2022Article
- Efficient suppression of parkinsonian beta oscillations in a closed-loop model of deep brain stimulation with amplitude modulation.Frontiers in human neuroscience · 2022Article
- Input Zone-Selective Dysrhythmia in Motor Thalamus after Dopamine Depletion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Computational investigation of the impact of deep brain stimulation contact size and shape on neural selectivity.Journal of neural engineering · 2021Article
- Bilateral Intracranial Beta Activity During Forced and Spontaneous Movements in a 6-OHDA Hemi-PD Rat Model.Frontiers in neuroscience · 2021Article
- Neural activity during a simple reaching task in macaques is counter to gating and rebound in basal ganglia-thalamic communication.PLoS biology · 2020Article
- Simulation of Closed-Loop Deep Brain Stimulation Control Schemes for Suppression of Pathological Beta Oscillations in Parkinson's Disease.Frontiers in neuroscience · 2020Article
- Electrodeposited platinum-iridium coating improves in vivo recording performance of chronically implanted microelectrode arrays.Biomaterials · 2019Article
- Effects of subthalamic deep brain stimulation on striatal metabolic connectivity in a rat hemiparkinsonian model.Disease models & mechanisms · 2019Article
- Deep cerebellar stimulation reduces ataxic motor symptoms in the shaker rat.Annals of neurology · 2019Article
- Biomarkers and Stimulation Algorithms for Adaptive Brain Stimulation.Frontiers in neuroscience · 2017Review
- A Network Model of Local Field Potential Activity in Essential Tremor and the Impact of Deep Brain Stimulation.PLoS computational biology · 2017Article
- Deep brain stimulation exacerbates hypokinetic dysarthria in a rat model of Parkinson's disease.Journal of neuroscience research · 2016Article
- Information in pallidal neurons increases with parkinsonian severity.Parkinsonism & related disorders · 2015Article
- Basal ganglia-thalamus and the "crowning enigma".Frontiers in neural circuits · 2015Review
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The degeneration of dopaminergic neurons in the substantia nigra pars compacta leads to parkinsonian motor symptoms via changes in electrophysiological activity throughout the basal ganglia. High-frequency deep brain stimulation (DBS) partially treats these symptoms, but the mechanisms are unclear. We hypothesize that motor symptoms of Parkinson's disease (PD) are associated with increased information transmission from basal ganglia output neurons to motor thalamus input neurons and that therapeutic DBS of the subthalamic nucleus (STN) treats these symptoms by reducing this extraneous information transmission. We tested these hypotheses in a unilateral, 6-hydroxydopamine-lesioned rodent model of hemiparkinsonism. Information transfer between basal ganglia output neurons and motor thalamus input neurons increased in both the orthodromic and antidromic directions with hemiparkinsonian (hPD) onset, and these changes were reversed by behaviorally therapeutic STN-DBS. Omnidirectional information increases in the parkinsonian state underscore the detrimental nature of that pathological information and suggest a loss of information channel independence. Therapeutic STN-DBS reduced that pathological information, suggesting an effective increase in the number of independent information channels. We interpret these data with a model in which pathological information and fewer information channels diminishes the scope of possible motor activities, driving parkinsonian symptoms. In this model, STN-DBS restores information-channel independence by eliminating or masking the parkinsonism-associated information, and thus enlarges the scope of possible motor activities, alleviating parkinsonian symptoms.
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