ArticleLife science alliance2024
Distinct calcium sources regulate temporal profiles of NMDAR and mGluR-mediated protein synthesis.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Gene expression regulation by CaCellular & molecular biology letters · 2026Pooled it
- Calcium dysregulation in neurovascular function in Alzheimer's disease: mechanisms, therapeutic targets.GeroScience · 2026Review
- Structural Neurotoxic and Neuroprotective Effects of Ketamine and Esketamine in Preclinical and Human Studies: A Systematic Review.Research square · 2026Article
- Group 1 mGluR stimulation rescues APOE4-mediated translation defects in neurons.Life science alliance · 2026Article
- Dysregulated mRNA Translation in Alzheimer's Disease: Mechanisms, Therapeutic Opportunities, and Challenges for Clinical Translation.Clinical interventions in aging · 2026Review
- Altering rRNA 2'O-methylation pattern during neuronal differentiation is regulated by FMRP.RNA biology · 2025Article
- Environmentally relevant lead exposure impacts gene expression in SH-SY5Y cells throughout neuronal differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- A review on recent advances in Alzheimer's disease: The role of synaptic plasticity.AIMS neuroscience · 2025Review
- Chemogenetic activation of Gq signaling modulates dendritic development of cortical neurons in a time- and layer-specific manner.Frontiers in cellular neuroscience · 2025Article
- Synaptopodin: a key regulator of Hebbian plasticity.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium signaling is integral for neuronal activity and synaptic plasticity. We demonstrate that the calcium response generated by different sources modulates neuronal activity-mediated protein synthesis, another process essential for synaptic plasticity. Stimulation of NMDARs generates a protein synthesis response involving three phases-increased translation inhibition, followed by a decrease in translation inhibition, and increased translation activation. We show that these phases are linked to NMDAR-mediated calcium response. Calcium influx through NMDARs elicits increased translation inhibition, which is necessary for the successive phases. Calcium through L-VGCCs acts as a switch from translation inhibition to the activation phase. NMDAR-mediated translation activation requires the contribution of L-VGCCs, RyRs, and SOCE. Furthermore, we show that IP3-mediated calcium release and SOCE are essential for mGluR-mediated translation up-regulation. Finally, we signify the relevance of our findings in the context of Alzheimer's disease. Using neurons derived from human fAD iPSCs and transgenic AD mice, we demonstrate the dysregulation of NMDAR-mediated calcium and translation response. Our study highlights the complex interplay between calcium signaling and protein synthesis, and its implications in neurodegeneration.
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