ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 36 citations in OpenAlex.
- Movement-related activity in the internal globus pallidus of the parkinsonian macaque.Journal of neurophysiology · 2025Article
- Neuronal Firing and Glutamatergic Synapses in the Substantia Nigra Pars Reticulata of LRRK2-G2019S Mice.Biomolecules · 2022Article
- Synaptic reshaping of plastic neuronal networks by periodic multichannel stimulation with single-pulse and burst stimuli.PLoS computational biology · 2022Article
- Distinct neuronal excitability alterations of medial prefrontal cortex in early-life neglect model of rats.Animal models and experimental medicine · 2022Article
- Protective effect of curcumin against rotenone-induced substantia nigra pars compacta neuronal dysfunction.Metabolic brain disease · 2022Article
- Spike-Timing-Dependent Plasticity Mediated by Dopamine and its Role in Parkinson's Disease Pathophysiology.Frontiers in network physiology · 2022Review
- Inhibitory Spike-Timing-Dependent Plasticity Can Account for Pathological Strengthening of Pallido-Subthalamic Synapses in Parkinson's Disease.Frontiers in physiology · 2022Article
- Early-Life Neglect Alters Emotional and Cognitive Behavior in a Sex-Dependent Manner and Reduces Glutamatergic Neuronal Excitability in the Prefrontal Cortex.Frontiers in psychiatry · 2020Article
- Cellular and Synaptic Dysfunctions in Parkinson's Disease: Stepping out of the Striatum.Cells · 2019Review
- Proliferation of Inhibitory Input to the Substantia Nigra in Experimental Parkinsonism.Frontiers in cellular neuroscience · 2019Article
- Dopamine Selectively Modulates the Outcome of Learning Unnatural Action-Valence Associations.Journal of cognitive neuroscience · 2017Article
- Stem Cell-Induced Biobridges as Possible Tools to Aid Neuroreconstruction after CNS Injury.Frontiers in cell and developmental biology · 2017Review
- Ventral Medial Thalamic Nucleus Promotes Synchronization of Increased High Beta Oscillatory Activity in the Basal Ganglia-Thalamocortical Network of the Hemiparkinsonian Rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Bursting activity of substantia nigra pars reticulata neurons in mouse parkinsonism in awake and anesthetized states.Neurobiology of disease · 2015Article
- Abnormal Bursting as a Pathophysiological Mechanism in Parkinson's Disease.Basal ganglia · 2014Article
- High and low frequency stimulation of the subthalamic nucleus induce prolonged changes in subthalamic and globus pallidus neurons.Frontiers in systems neuroscience · 2013Article
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Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impairments of synaptic plasticity are a hallmark of several neurological disorders, including Parkinson's disease (PD) which results from the progressive loss of dopaminergic neurons of the substantia nigra pars compacta leading to abnormal activity within the basal ganglia (BG) network and pathological motor symptoms. Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of the BG, is correlated to the onset of PD-related movement disorders and thus has been proposed to be a key neural substrate regulating information flow and motor function in BG circuits. However, a critical question is whether similar plasticity impairments could occur at other glutamatergic connections within the BG that would also affect the inhibitory influence of the network on the motor thalamus. Here, we show that long-term plasticity at subthalamo-nigral glutamatergic synapses (STN-SNr) sculpting the activity patterns of nigral neurons, the main output of the network, is also affected in experimental parkinsonism. Using whole-cell patch-clamp in acute rat brain slices, we describe a molecular pathway supporting an activity-dependent long-term depression of STN-SNr synapses through an NMDAR-and D1/5 dopamine receptor-mediated endocytosis of synaptic AMPA glutamate receptors. We also show that this plastic property is lost in an experimental rat model of PD but can be restored through the recruitment of dopamine D1/5 receptors. Altogether, our findings suggest that pathological impairments of subthalamo-nigral plasticity may enhance BG outputs and thereby contribute to PD-related motor dysfunctions.
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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.