ArticleScientific reports2018
Impact of Reduced Cerebellar EAAT Expression on Purkinje Cell Firing Pattern of NPC1-deficient Mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Modulation of glutamate metabolism in Niemann-pick disease type C1 mice.Molecular genetics and metabolism reports · 2026Article
- The Cerebellum in Niemann-Pick C1 Disease: Mouse Versus Man.Cerebellum (London, England) · 2023Review
- Article
- Reduction of glutamate neurotoxicity: A novel therapeutic approach for Niemann-Pick disease, type C1.Molecular genetics and metabolism · 2021Article
- Pluripotent Stem Cells for Disease Modeling and Drug Discovery in Niemann-Pick Type C1.International journal of molecular sciences · 2021Review
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- Single Cell Transcriptome Analysis of Niemann-Pick Disease, Type C1 Cerebella.International journal of molecular sciences · 2020Article
- Alteration of GABAergic Input Precedes Neurodegeneration of Cerebellar Purkinje Cells of NPC1-Deficient Mice.International journal of molecular sciences · 2019Article
- Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System.International journal of molecular sciences · 2019Review
- Electrophysiological Excitability and Parallel Fiber Synaptic Properties of Zebrin-Positive and -Negative Purkinje Cells in Lobule VIII of the Mouse Cerebellar Slice.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Niemann-Pick disease Type C1 (NPC1) is a rare hereditary neurodegenerative disease. NPC1-patients suffer, amongst others, from ataxia, based on a loss of cerebellar Purkinje cells (PCs). Impaired expression/function of excitatory amino acid transporters (EAATs) are suspected of contributing to PC-degeneration in hereditary spinocerebellar ataxias (SCAs). Thus, we studied EAAT-expression and its impact to PC-activity in NPC1
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