ArticleNeuron2017
Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following Degeneration of Midbrain Dopamine Neurons.
Article in Neuron, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Connectivity and Functionality of the Globus Pallidus Externa Under Normal Conditions and Parkinson's Disease.Frontiers in neural circuits · 2021Pooled it
- The promotion-like effect of the M1-STN hyperdirect pathway induced by ccPAS enhanced balance performances: From the perspective of brain connectivity.CNS neuroscience & therapeutics · 2024Trial
- Nigra-Subthalamic Dopaminergic Circuitry Modulates and Represents Distinct Pain Modality in Physiological and Pain States in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emergence of Task-Related Motor Cortical Dysfunction in Mice with Progressive Parkinsonism.bioRxiv : the preprint server for biology · 2026Article
- Calcium-based synaptic and structural plasticity link pathological activity to synaptic reorganization in Parkinson's disease.Science advances · 2025Article
- Dysfunction of subthalamic dopaminergic circuitry contributes to anxiety- and depression-like behaviors in 6-OHDA lesion-induced hemiparkinsonian mice.Acta pharmacologica Sinica · 2025Article
- The association between infant EEG aperiodic exponent and the trajectory of restricted and repetitive behaviors for toddlers with and without autism.Journal of neurodevelopmental disorders · 2025Article
- Enhanced beta power emerges from simulated parkinsonian primary motor cortex.NPJ Parkinson's disease · 2025Article
- Article
- Movement-related activity in the internal globus pallidus of the parkinsonian macaque.Journal of neurophysiology · 2025Article
- Delay suppression control of β-oscillations: a proposal for dual-target adaptive deep brain stimulation on STN-GPe network model.Biological cybernetics · 2025Article
- Enhanced beta power emerges from simulated parkinsonian primary motor cortex.bioRxiv : the preprint server for biology · 2025Article
- Corticostriatal glutamate-mediated dynamic therapeutic efficacy of electroacupuncture in a parkinsonian rat model.Clinical and translational medicine · 2024Article
- Neuroplasticity in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Neural indices of heritable impulsivity: Impact of the COMT Val158Met polymorphism on frontal beta power during early motor preparation.Biological psychology · 2024Article
- Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024Review
- Synaptic reorganization of synchronized neuronal networks with synaptic weight and structural plasticity.PLoS computational biology · 2024Article
- Optimization of an anatomically and electrically detailed rodent subthalamic nucleus neuron model.Journal of neurophysiology · 2024Article
- Medication-invariant resting aperiodic and periodic neural activity in Parkinson's disease.Psychophysiology · 2024Article
- Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The motor symptoms of Parkinson's disease (PD) are linked to abnormally correlated and coherent activity in the cortex and subthalamic nucleus (STN). However, in parkinsonian mice we found that cortico-STN transmission strength had diminished by 50%-75% through loss of axo-dendritic and axo-spinous synapses, was incapable of long-term potentiation, and less effectively patterned STN activity. Optogenetic, chemogenetic, genetic, and pharmacological interrogation suggested that downregulation of cortico-STN transmission in PD mice was triggered by increased striato-pallidal transmission, leading to disinhibition of the STN and increased activation of STN NMDA receptors. Knockdown of STN NMDA receptors, which also suppresses proliferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN transmission and patterning and improved motor function. Together, the data suggest that loss of dopamine triggers a maladaptive shift in the balance of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and motor dysfunction.
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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.