ArticleeLife2019
State transitions in the substantia nigra reticulata predict the onset of motor deficits in models of progressive dopamine depletion in mice.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- Astrocytes mediate the dopaminergic modulation of tonic GABAergic signaling in substantia nigra.Science advances · 2026Article
- Emergence of Task-Related Motor Cortical Dysfunction in Mice with Progressive Parkinsonism.bioRxiv : the preprint server for biology · 2026Article
- Tissue Effects of the Mitochondrial Division Inhibitor Mdivi-1 on the Substantia Nigra in a Laboratory Model of Dopaminergic System Damage.International journal of molecular sciences · 2026Article
- Braking Parkinson's progression: the hypothetical druggable role of striatal parvalbumin interneurons.NPJ Parkinson's disease · 2026Review
- Exercise evokes retained motor performance without neuroprotection in a mouse model of Parkinson's disease.Frontiers in physiology · 2026Article
- Synaptic integration and competition in the substantia nigra pars reticulata-An experimental and in silico analysis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Calcium-based synaptic and structural plasticity link pathological activity to synaptic reorganization in Parkinson's disease.Science advances · 2025Article
- Movement-related activity in the internal globus pallidus of the parkinsonian macaque.Journal of neurophysiology · 2025Article
- Exosomes as Biomarkers and Therapeutic Agents in Neurodegenerative Diseases: Current Insights and Future Directions.Molecular neurobiology · 2025Review
- Motor cortical neuronal hyperexcitability associated with α-synuclein aggregation.NPJ Parkinson's disease · 2025Article
- Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation.Research square · 2024Article
- Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation.bioRxiv : the preprint server for biology · 2024Article
- Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024Review
- Dopamine depletion weakens direct pathway modulation of SNr neurons.Neurobiology of disease · 2024Article
- Synaptic Changes in Pallidostriatal Circuits Observed in the Parkinsonian Model Triggers Abnormal Beta Synchrony with Accurate Spatio-temporal Properties across the Basal Ganglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The onset of motor learning impairments in Parkinson's disease: a computational investigation.Brain informatics · 2024Article
- Dopamine Signaling in Substantia Nigra and Its Impact on Locomotor Function-Not a New Concept, but Neglected Reality.International journal of molecular sciences · 2024Review
- Automated procedure to detect subtle motor alterations in the balance beam test in a mouse model of early Parkinson's disease.Scientific reports · 2024Article
- Article
- Substantia Nigra Pars Reticulata Projections to the Pedunculopontine Nucleus Modulate Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder whose cardinal motor symptoms are attributed to dysfunction of basal ganglia circuits under conditions of low dopamine. Despite well-established physiological criteria to define basal ganglia dysfunction, correlations between individual parameters and motor symptoms are often weak, challenging their predictive validity and causal contributions to behavior. One limitation is that basal ganglia pathophysiology is studied only at end-stages of depletion, leaving an impoverished understanding of when deficits emerge and how they evolve over the course of depletion. In this study, we use toxin- and neurodegeneration-induced mouse models of dopamine depletion to establish the physiological trajectory by which the substantia nigra reticulata (SNr) transitions from the healthy to the diseased state. We find that physiological progression in the SNr proceeds in discrete state transitions that are highly stereotyped across models and correlate well with the prodromal and symptomatic stages of behavior.
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Registered trials
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.