ArticleFrontiers in cellular neuroscience2016
Abnormal Development of Glutamatergic Synapses Afferent to Dopaminergic Neurons of the Pink1(-/-) Mouse Model of Parkinson's Disease.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- Synapses-associated research in Parkinson's disease: an explored trends analysis.Frontiers in aging neuroscience · 2025Article
- Endogenous PTEN-Induced Kinase 1 Regulates Dendritic Architecture and Spinogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Pathophysiological Features of Nigral Dopaminergic Neurons in Animal Models of Parkinson's Disease.International journal of molecular sciences · 2022Review
- Genes Implicated in Familial Parkinson's Disease Provide a Dual Picture of Nigral Dopaminergic Neurodegeneration with Mitochondria Taking Center Stage.International journal of molecular sciences · 2021Review
- PINK1 Silencing Modifies Dendritic Spine Dynamics of Mouse Hippocampal Neurons.Journal of molecular neuroscience : MN · 2019Article
- SerThr-PhosphoProteome of Brain from Aged PINK1-KO+A53T-SNCA Mice Reveals pT1928-MAP1B and pS3781-ANK2 Deficits, as Hub between Autophagy and Synapse Changes.International journal of molecular sciences · 2019Article
- Presynaptic Dysfunction by Familial Factors in Parkinson Disease.International neurourology journal · 2018Article
- Liver X Receptor Agonist GW3965 Regulates Synaptic Function upon Amyloid Beta Exposure in Hippocampal Neurons.Neurotoxicity research · 2018Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a preceding study, we showed that in adult pink1(-/-) mice, a monogenic animal model of Parkinson's disease (PD), striatal neurons display aberrant electrical activities that precede the onset of overt clinical manifestations. Here, we tested the hypothesis that the maturation of dopaminergic (DA) neurons of the pink1(-/-) substantia nigra compacta (SNc) follows, from early stages on, a different developmental trajectory from age-matched wild type (wt) SNc DA neurons. We used immature (postnatal days P2-P10) and young adult (P30-P90) midbrain slices of pink1(-/-) mice expressing the green fluorescent protein in tyrosine hydroxylase (TH)-positive neurons. We report that the developmental sequence of N-Methyl-D-aspartic acid (NMDA) spontaneous excitatory postsynaptic currents (sEPSCs) is altered in pink1(-/-) SNc DA neurons, starting from shortly after birth. They lack the transient episode of high NMDA receptor-mediated neuronal activity characteristic of the immature stage of wt SNc DA neurons. The maturation of the membrane resistance of pink1(-/-) SNc DA neurons is also altered. Collectively, these observations suggest that electrical manifestations occurring shortly after birth in SNc DA neurons might lead to dysfunction in dopamine release and constitute an early pathogenic mechanism of PD.
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