ArticleProceedings of the National Academy of Sciences of the United States of America2011
Beta Ca2+/CaM-dependent kinase type II triggers upregulation of GluA1 to coordinate adaptation to synaptic inactivity in hippocampal neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Synaptic homeostasis transiently leverages Hebbian mechanisms for a multiphasic response to inactivity.Cell reports · 2024Article
- Sex difference in the effect of environmental enrichment on food restriction-induced persistence of cocaine conditioned place preference and mechanistic underpinnings.Addiction neuroscience · 2024Article
- Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Heterogeneous CaMKII-Dependent Synaptic Compensations in CA1 Pyramidal Neurons From Acute Hippocampal Slices.Frontiers in cellular neuroscience · 2022Article
- Review
- Homeostatic regulation of reward via synaptic insertion of calcium-permeable AMPA receptors in nucleus accumbens.Physiology & behavior · 2020Review
- Phosphorylation-Dependent Regulation of CaFrontiers in synaptic neuroscience · 2020Article
- Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Homeostatic synaptic scaling: molecular regulators of synaptic AMPA-type glutamate receptors.F1000Research · 2018Review
- Synaptic homeostasis requires the membrane-proximal carboxy tail of GluA2.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- A microRNA-129-5p/Rbfox crosstalk coordinates homeostatic downscaling of excitatory synapses.The EMBO journal · 2017Article
- Neuropeptide VGF Promotes Maturation of Hippocampal Dendrites That Is Reduced by Single Nucleotide Polymorphisms.International journal of molecular sciences · 2017Article
- Miro1-dependent mitochondrial positioning drives the rescaling of presynaptic Ca2+ signals during homeostatic plasticity.EMBO reports · 2017Article
- Gestational Hypothyroxinemia Affects Glutamatergic Synaptic Protein Distribution and Neuronal Plasticity Through Neuron-Astrocyte Interplay.Molecular neurobiology · 2016Article
- Fine-tuning of synaptic upscaling at excitatory synapses by endocannabinoid signaling is mediated via the CB1 receptor.Scientific reports · 2015Article
- Postsynaptic VAMP/Synaptobrevin Facilitates Differential Vesicle Trafficking of GluA1 and GluA2 AMPA Receptor Subunits.PloS one · 2015Article
- Modulation of network activity and induction of homeostatic synaptic plasticity by enzymatic removal of heparan sulfates.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolonged AMPA-receptor blockade in hippocampal neuron cultures leads to both an increased expression of GluA1 postsynaptically and an increase in vesicle pool size and turnover rate presynaptically, adaptive changes that extend beyond simple synaptic scaling. As a molecular correlate, expression of the β Ca(2+)/CaM-dependent kinase type II (βCaMKII) is increased in response to synaptic inactivity. Here we set out to clarify the role of βCaMKII in the various manifestations of adaptation. Knockdown of βCaMKII by lentiviral-mediated expression of shRNA prevented the synaptic inactivity-induced increase in GluA1, as did treatment with the CaM kinase inhibitor KN-93, but not the inactive analog KN-92. These results demonstrate that, spurred by AMPA-receptor blockade, up-regulation of βCaMKII promotes increased GluA1 expression. Indeed, transfection of βCaMKII, but not a kinase-dead mutant, increased GluA1 expression on dendrites and elevated vesicle turnover (Syt-Ab uptake), mimicking the effect of synaptic inactivity on both sides of the synapse. In cells with elevated βCaMKII, relief of synaptic-activity blockade uncovered an increase in the frequency of miniature excitatory postsynaptic currents that could be rapidly and fully suppressed by PhTx blockade of GluA1 receptors. This increased mini frequency involved a genuine presynaptic enhancement, not merely an increased abundance of synapses. This finding suggests that Ca(2+) flux through GluA1 receptors may trigger the acute release of a retrograde messenger. Taken together, our results indicate that synaptic inactivity-induced increases in βCaMKII expression set in motion a series of events that culminate in coordinated pre- and postsynaptic adaptations in synaptic transmission.
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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.