ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Mutant PKCγ in spinocerebellar ataxia type 14 disrupts synapse elimination and long-term depression in Purkinje cells in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 83 citations in OpenAlex.
- Loss of YY1 in Purkinje cells triggers cerebellar ataxia via Wnt10b-mediated impairment of dendrite development.iScience · 2026Article
- Enhanced mGluR1 function causes motor deficits and region-specific Purkinje cell dysfunction.Brain : a journal of neurology · 2026Article
- Sex-specific disruptions in PKCγ signaling in a mouse model of spinocerebellar ataxia type 14.JCI insight · 2026Article
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Article
- Pre-ataxic loss of intrinsic plasticity and motor learning in a mouse model of SCA1.Brain : a journal of neurology · 2023Article
- O-GlcNAcylation Is Required for the Survival of Cerebellar Purkinje Cells by Inhibiting ROS Generation.Antioxidants (Basel, Switzerland) · 2023Article
- Viewpoint: spinocerebellar ataxias as diseases of Purkinje cell dysfunction rather than Purkinje cell loss.Frontiers in molecular neuroscience · 2023Review
- Article
- Electrophysiological and Imaging Analysis of GFP-Tagged Protein Kinase C γ Translocation in Cerebellar Purkinje Cells.Cerebellum (London, England) · 2022Article
- Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications.Cerebellum (London, England) · 2022Article
- TRPC3 Channel Activity and Viability of Purkinje Neurons can be Regulated by a Local Signalosome.Frontiers in molecular biosciences · 2022Article
- Two Sides of the Same Coin: Protein Kinase C γ in Cancer and Neurodegeneration.Frontiers in cell and developmental biology · 2022Review
- W246G Mutant ELOVL4 Impairs Synaptic Plasticity in Parallel and Climbing Fibers and Causes Motor Defects in a Rat Model of SCA34.Molecular neurobiology · 2021Article
- A New Mouse Model Related to SCA14 Carrying a Pseudosubstrate Domain Mutation in PKCγ Shows Perturbed Purkinje Cell Maturation and Ataxic Motor Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Cerebellar developmental deficits underlie neurodegenerative disorder spinocerebellar ataxia type 23.Brain pathology (Zurich, Switzerland) · 2021Article
- Precise Regulation of the Basal PKCγ Activity by DGKγ Is Crucial for Motor Coordination.International journal of molecular sciences · 2020Article
- Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice.Investigative ophthalmology & visual science · 2020Article
- Aberrant Cerebellar Circuitry in the Spinocerebellar Ataxias.Frontiers in neuroscience · 2020Review
- Cerebellar Development and Circuit Maturation: A Common Framework for Spinocerebellar Ataxias.Frontiers in neuroscience · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Cerebellar Purkinje cells (PCs) express a large amount of the γ isoform of protein kinase C (PKCγ) and a modest level of PKCα. The PKCγ is involved in the pruning of climbing fiber (CF) synapses from developing PCs, and PKCα plays a critical role in long-term depression (LTD) at parallel fiber (PF)-PC synapses. Moreover, the PKC signaling in PCs negatively modulates the nonselective transient receptor potential cation channel type 3 (TRPC3), the opening of which elicits slow EPSCs at PF-PC synapses. Autosomal dominant spinocerebellar ataxia type 14 (SCA14) is caused by mutations in PKCγ. To clarify the pathology of this disorder, mutant (S119P) PKCγ tagged with GFP was lentivirally expressed in developing and mature mouse PCs in vivo, and the effects were assessed 3 weeks after the injection. Mutant PKCγ-GFP aggregated in PCs without signs of degeneration. Electrophysiology results showed impaired pruning of CF synapses from developing PCs, failure of LTD expression, and increases in slow EPSC amplitude. We also found that mutant PKCγ colocalized with wild-type PKCγ, which suggests that mutant PKCγ acts in a dominant-negative manner on wild-type PKCγ. In contrast, PKCα did not colocalize with mutant PKCγ. The membrane residence time of PKCα after depolarization-induced translocation, however, was significantly decreased when it was present with the mutant PKCγ construct. These results suggest that mutant PKCγ in PCs of SCA14 patients could differentially impair the membrane translocation kinetics of wild-type γ and α PKCs, which would disrupt synapse pruning, synaptic plasticity, and synaptic transmission.
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