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Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations.
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Merkel Cells Activate Sensory Neural Pathways through Adrenergic Synapses.
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Evoked transients of pH-sensitive fluorescent false neurotransmitter reveal dopamine hot spots in the globus pallidus.
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Dopamine Triggers the Maturation of Striatal Spiny Projection Neuron Excitability during a Critical Period.
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Designing a norepinephrine optical tracer for imaging individual noradrenergic synapses and their activity in vivo.
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Neuromelanin organelles are specialized autolysosomes that accumulate undegraded proteins and lipids in aging human brain and are likely involved in Parkinson's disease.
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Toward Serotonin Fluorescent False Neurotransmitters: Development of Fluorescent Dual Serotonin and Vesicular Monoamine Transporter Substrates for Visualizing Serotonin Neurons.
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Identification of Fluorescent Small Molecule Compounds for Synaptic Labeling by Image-Based, High-Content Screening.
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Neuromelanin detection by magnetic resonance imaging (MRI) and its promise as a biomarker for Parkinson's disease.
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An Easy-to-Implement Protocol for Preparing Postnatal Ventral Mesencephalic Cultures.
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Piezo High Accuracy Surgical Osteal Removal (PHASOR): A Technique for Improved Cranial Window Surgery in Mice.
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Dopamine's Effects on Corticostriatal Synapses during Reward-Based Behaviors.
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Synaptic plasticity may underlie l-DOPA induced dyskinesia.
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Neuroprotection and neurorestoration as experimental therapeutics for Parkinson's disease.
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α-Synuclein-Dependent Calcium Entry Underlies Differential Sensitivity of Cultured SN and VTA Dopaminergic Neurons to a Parkinsonian Neurotoxin.
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Neuronal Depolarization Drives Increased Dopamine Synaptic Vesicle Loading via VGLUT.
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T cells from patients with Parkinson's disease recognize α-synuclein peptides.
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Dopamine release from the locus coeruleus to the dorsal hippocampus promotes spatial learning and memory.
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Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation.
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Parkinsonism Driven by Antipsychotics Originates from Dopaminergic Control of Striatal Cholinergic Interneurons.
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Fluorescent false neurotransmitter reveals functionally silent dopamine vesicle clusters in the striatum.
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Mechanisms of amphetamine action illuminated through optical monitoring of dopamine synaptic vesicles in Drosophila brain.
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Loss of VGLUT3 Produces Circadian-Dependent Hyperdopaminergia and Ameliorates Motor Dysfunction and l-Dopa-Mediated Dyskinesias in a Model of Parkinson's Disease.
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