ArticleMovement disorders : official journal of the Movement Disorder Society2014
PINK1 heterozygous mutations induce subtle alterations in dopamine-dependent synaptic plasticity.
Article in Movement disorders : official journal of the Movement Disorder Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- Upregulated ECM genes and increased synaptic activity in Parkinson's human DA neurons with PINK1/ PRKN mutations.NPJ Parkinson's disease · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Vitamin E and Its Molecular Effects in Experimental Models of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Neuropathology of incidental Lewy body & prodromal Parkinson's disease.Molecular neurodegeneration · 2023Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Pattern of Mitochondrial Respiration in Peripheral Blood Cells of Patients with Parkinson's Disease.International journal of molecular sciences · 2022Article
- Estrogen-related receptor gamma regulates mitochondrial and synaptic genes and modulates vulnerability to synucleinopathy.NPJ Parkinson's disease · 2022Article
- PINK1 antagonize intracerebral hemorrhage by promoting mitochondrial autophagy.Annals of clinical and translational neurology · 2021Article
- Progressive parkinsonism due to mitochondrial impairment: Lessons from the MitoPark mouse model.Experimental neurology · 2021Review
- Increased glutamate transmission onto dorsal striatum spiny projection neurons in Pink1 knockout rats.Neurobiology of disease · 2021Article
- Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats.Frontiers in neuroscience · 2021Article
- Synaptic Changes in Parkinson Disease Assessed with in vivo Imaging.Annals of neurology · 2020Article
- PINK1 Silencing Modifies Dendritic Spine Dynamics of Mouse Hippocampal Neurons.Journal of molecular neuroscience : MN · 2019Article
- Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson's Disease.International journal of molecular sciences · 2019Article
- Dietary Vitamin E as a Protective Factor for Parkinson's Disease: Clinical and Experimental Evidence.Frontiers in neurology · 2019Article
- Spiny Projection Neuron Dynamics in Toxin and Transgenic Models of Parkinson's Disease.Frontiers in neural circuits · 2019Review
- Synaptic Plasticity Changes: Hallmark for Neurological and Psychiatric Disorders.Neural plasticity · 2018Article
- Centrality of Early Synaptopathy in Parkinson's Disease.Frontiers in neurology · 2018Review
- Progression of pathology in PINK1-deficient mouse brain from splicing via ubiquitination, ER stress, and mitophagy changes to neuroinflammation.Journal of neuroinflammation · 2017Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Homozygous or compound heterozygous mutations in the phosphatase and tensin homolog-induced putative kinase 1 (PINK1) gene are causative of autosomal recessive, early onset Parkinson's disease. Single heterozygous mutations have been detected repeatedly both in a subset of patients and in unaffected individuals, and the significance of these mutations has long been debated. Several neurophysiological studies from non-manifesting PINK1 heterozygotes have demonstrated the existence of neural plasticity abnormalities, indicating the presence of specific endophenotypic traits in the heterozygous state. We performed a functional analysis of corticostriatal synaptic plasticity in heterozygous PINK1 knockout (PINK1(+/-) ) mice using a multidisciplinary approach and observed that, despite normal motor behavior, repetitive activation of cortical inputs to striatal neurons failed to induce long-term potentiation (LTP), whereas long-term depression was normal. Although nigral dopaminergic neurons exhibited normal morphological and electrophysiological properties with normal responses to dopamine receptor activation, a significantly lower dopamine release was measured in the striatum of PINK1(+/-) mice compared with control mice, suggesting that a decrease in stimulus-evoked dopamine overflow acts as a major determinant for the LTP deficit. Accordingly, pharmacological agents capable of increasing the availability of dopamine in the synaptic cleft restored normal LTP in heterozygous mice. Moreover, monoamine oxidase B inhibitors rescued physiological LTP and normal dopamine release. Our results provide novel evidence for striatal plasticity abnormalities, even in the heterozygous disease state. These alterations might be considered an endophenotype to this monogenic form of Parkinson's disease and a valid tool with which to characterize early disease stage and design possible disease-modifying therapies.
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