ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Proliferation of external globus pallidus-subthalamic nucleus synapses following degeneration of midbrain dopamine neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Connectivity and Functionality of the Globus Pallidus Externa Under Normal Conditions and Parkinson's Disease.Frontiers in neural circuits · 2021Pooled it
- Article
- Emergence of Task-Related Motor Cortical Dysfunction in Mice with Progressive Parkinsonism.bioRxiv : the preprint server for biology · 2026Article
- Susceptibility and diffusion MRI biomarkers predict development of Parkinsonism in iRBD.NPJ Parkinson's disease · 2025Article
- Calcium-based synaptic and structural plasticity link pathological activity to synaptic reorganization in Parkinson's disease.Science advances · 2025Article
- Enhanced beta power emerges from simulated parkinsonian primary motor cortex.NPJ Parkinson's disease · 2025Article
- Enhanced beta power emerges from simulated parkinsonian primary motor cortex.bioRxiv : the preprint server for biology · 2025Article
- Unraveling the Complexity of Parkinson's Disease: Insights into Pathogenesis and Precision Interventions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Computational study of associations between the synaptic conductance of STN and GPe and the development of Parkinson's disease.Cognitive neurodynamics · 2024Article
- Synchronization of delayed coupled neurons with multiple synaptic connections.Cognitive neurodynamics · 2024Article
- Article
- 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
- Non-Faradaic optoelectrodes for safe electrical neuromodulation.Nature communications · 2024Article
- Coordinated reset stimulation of plastic neural networks with spatially dependent synaptic connections.Frontiers in network physiology · 2024Article
- Dynamics of parkinsonian oscillations mediated by transmission delays in a mean-field model of the basal ganglia.Frontiers in cellular neuroscience · 2024Article
- The transcription regulator Lmo3 is required for the development of medial ganglionic eminence derived neurons in the external globus pallidus.Developmental biology · 2023Article
- Altered Thalamocortical Signaling in a Mouse Model of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Cell and circuit complexity of the external globus pallidus.Nature neuroscience · 2023Review
- Exploration behavior after reversals is predicted by STN-GPe synaptic plasticity in a basal ganglia model.iScience · 2023Article
- Basal ganglia neurons in healthy and parkinsonian primates generate recurring sequences of spikes.Journal of neurophysiology · 2023Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The symptoms of Parkinson's disease (PD) are related to changes in the frequency and pattern of activity in the reciprocally connected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN). In idiopathic and experimental PD, the GPe and STN exhibit hypoactivity and hyperactivity, respectively, and abnormal synchronous rhythmic burst firing. Following lesion of midbrain dopamine neurons, abnormal STN activity emerges slowly and intensifies gradually until it stabilizes after 2-3 weeks. Alterations in cellular/network properties may therefore underlie the expression of abnormal firing. Because the GPe powerfully regulates the frequency, pattern, and synchronization of STN activity, electrophysiological, molecular, and anatomical measures of GPe-STN transmission were compared in the STN of control and 6-hydroxydopamine-lesioned rats and mice. Following dopamine depletion: (1) the frequency (but not the amplitude) of mIPSCs increased by ∼70%; (2) the amplitude of evoked IPSCs and isoguvacine-evoked current increased by ∼60% and ∼70%, respectively; (3) mRNA encoding α1, β2, and γ2 GABA(A) receptor subunits increased by 15-30%; (4) the density of postsynaptic gephyrin and γ2 subunit coimmunoreactive structures increased by ∼40%, whereas the density of vesicular GABA transporter and bassoon coimmunoreactive axon terminals was unchanged; and (5) the number of ultrastructurally defined synapses per GPe-STN axon terminal doubled with no alteration in terminal/synapse size or target preference. Thus, loss of dopamine leads, through an increase in the number of synaptic connections per GPe-STN axon terminal, to substantial strengthening of the GPe-STN pathway. This adaptation may oppose hyperactivity but could also contribute to abnormal firing patterns in the parkinsonian STN.
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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.