ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Involvement of protein synthesis and degradation in long-term potentiation of Schaffer collateral CA1 synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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89 citing papers in PubMed, 163 citations in OpenAlex.
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- Keeping synapses in shape: degradation pathways in the healthy and aging brain.Neuronal signaling · 2022Review
- A computational model of dopaminergic modulation of hippocampal Schaffer collateral-CA1 long-term plasticity.Journal of computational neuroscience · 2022Article
- The proteasome and its role in the nervous system.Cell chemical biology · 2021Review
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- Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Cdh1-APC Regulates Protein Synthesis and Stress Granules in Neurons through an FMRP-Dependent Mechanism.iScience · 2020Article
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- Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice.International journal of molecular sciences · 2019Article
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- Emerging Concepts and Functions of Autophagy as a Regulator of Synaptic Components and Plasticity.Cells · 2019Review
- Angelman syndrome-associated point mutations in the ZnThe Journal of biological chemistry · 2018Article
- Paradoxical LTP maintenance with inhibition of protein synthesis and the proteasome suggests a novel protein synthesis requirement for early LTP reversal.Journal of theoretical biology · 2018Article
- PA28αβ overexpression enhances learning and memory of female mice without inducing 20S proteasome activity.BMC neuroscience · 2018Article
- Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System.Journal of visualized experiments : JoVE · 2018Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of synaptic plasticity involves the translation of mRNA into protein and, probably, active protein degradation via the proteasome pathway. Here, we report on the rapid activation of synthesis and degradation of a probe protein with the induction of long-term potentiation (LTP) in the hippocampal Schaffer collateral CA1 pathway. The proteasome inhibitor MG132 significantly reduced the field EPSP slope potentiation and LTP maintenance without acutely affecting basal synaptic transmission. To visualize protein dynamics, CA1 pyramidal cells of hippocampal slices were transfected with Semliki Forest virus particles expressing a recombinant RNA. This RNA contained the coding sequence for a degradable green fluorescence protein with a nuclear localization signal (NLS-d1EGFP) followed by a 3'- untranslated region dendritic targeting sequence. NLS-d1EGFP fluorescence remained stable in the low-frequency test stimulation but increased with LTP induction in the cell body and in most dendritic compartments of CA1 neurons. Applying anisomycin, a protein synthesis inhibitor, caused NLS-d1EGFP levels to decline; a proteasome inhibitor MG132 reversed this effect. In the presence of anisomycin, LTP induction accelerated the degradation of NLS-d1EGFP. When both inhibitors were present, NLS-d1EGFP levels remained unaffected by LTP induction. Moreover, LTP-induced acceleration of NLS-d1EGFP synthesis was blocked by rapamycin, which is consistent with the involvement of dendritic mammalian target of rapamycin in LTP-triggered translational activity. Our results clearly demonstrate that LTP induction not only leads to a rapid increase in the rate of protein synthesis but also accelerates protein degradation via the proteasome system.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.