ArticleCommunications biology2020
PKN1 promotes synapse maturation by inhibiting mGluR-dependent silencing through neuronal glutamate transporter activation.
Article in Communications biology, 2020. 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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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Developmental pyrethroid exposure disrupts molecular pathways for MAP kinase and circadian rhythms in mouse brain.Physiological genomics · 2025Article
- Glucose-1,6-bisphosphate: A new gatekeeper of cerebral mitochondrial pyruvate uptake.Molecular metabolism · 2024Article
- Developmental pyrethroid exposure disrupts molecular pathways for MAP kinase and circadian rhythms in mouse brain.bioRxiv : the preprint server for biology · 2024Article
- EAAT3 impedes oligodendrocyte remyelination in chronic cerebral hypoperfusion-induced white matter injury.CNS neuroscience & therapeutics · 2024Article
- The role of PKN1 in glioma pathogenesis and the antiglioma effect of raloxifene targeting PKN1.Journal of cellular and molecular medicine · 2023Article
- Neural mechanism underlies CYLD modulation of morphology and synaptic function of medium spiny neurons in dorsolateral striatum.Frontiers in molecular neuroscience · 2023Article
- New perspectives on cytoskeletal dysregulation and mitochondrial mislocalization in amyotrophic lateral sclerosis.Translational neurodegeneration · 2021Review
- PKN1 Is a Novel Regulator of Hippocampal GluA1 Levels.Frontiers in synaptic neuroscience · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal metabotropic glutamate receptor (mGluR) activity could cause brain disorders; however, its regulation has not yet been fully understood. Here, we report that protein kinase N1 (PKN1), a protein kinase expressed predominantly in neurons in the brain, normalizes group 1 mGluR function by upregulating a neuronal glutamate transporter, excitatory amino acid transporter 3 (EAAT3), and supports silent synapse activation. Knocking out PKN1a, the dominant PKN1 subtype in the brain, unmasked abnormal input-nonspecific mGluR-dependent long-term depression (mGluR-LTD) and AMPA receptor (AMPAR) silencing in the developing hippocampus. mGluR-LTD was mimicked by inhibiting glutamate transporters in wild-type mice. Knocking out PKN1a decreased hippocampal EAAT3 expression and PKN1 inhibition reduced glutamate uptake through EAAT3. Also, synaptic transmission was immature; there were more silent synapses and fewer spines with shorter postsynaptic densities in PKN1a knockout mice than in wild-type mice. Thus, PKN1 plays a critical role in regulation of synaptic maturation by upregulating EAAT3 expression.
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Registered trials
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