ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
In vivo synaptic scaling is mediated by GluA2-lacking AMPA receptors in the embryonic spinal cord.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Lidocaine for Depressive Symptoms and Comorbid Pain: A Narrative Review of Mechanisms, Evidence, and Safety.Drug design, development and therapy · 2026Review
- Disuse plasticity limits spinal cord injury recovery.iScience · 2025Article
- 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
- A critical period for learning and plastic changes at hippocampal CA1 synapses.Scientific reports · 2022Article
- Article
- The Uniform and Nonuniform Nature of Slow and Rapid Scaling in Embryonic Motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?International journal of molecular sciences · 2021Review
- Divergent Synaptic Scaling of Miniature EPSCs following Activity Blockade in Dissociated Neuronal Cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Regulation of synaptic scaling by action potential-independent miniature neurotransmission.Journal of neuroscience research · 2018Review
- β-Amyloid triggers aberrant over-scaling of homeostatic synaptic plasticity.Acta neuropathologica communications · 2016Article
- Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- GluA4 subunit of AMPA receptors mediates the early synaptic response to altered network activity in the developing hippocampus.Journal of neurophysiology · 2016Article
- MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity.Nature communications · 2015Article
- Upward synaptic scaling is dependent on neurotransmission rather than spiking.Nature communications · 2015Article
- Spinal NMDA receptor activation constrains inactivity-induced phrenic motor facilitation in Charles River Sprague-Dawley rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Homeostatic synaptic plasticity in developing spinal networks driven by excitatory GABAergic currents.Neuropharmacology · 2014Review
- Article
- Review
- Persistent synaptic scaling independent of AMPA receptor subunit composition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
When spiking activity within a network is perturbed for hours to days, compensatory changes in synaptic strength are triggered that are thought to be important for the homeostatic maintenance of network or cellular spiking activity. In one form of this homeostatic plasticity, called synaptic scaling, all of a cell's AMPAergic miniature postsynaptic currents (mEPSCs) are increased or decreased by some scaling factor. Although synaptic scaling has been observed in a variety of systems, the mechanisms that underlie AMPAergic scaling have been controversial. Certain studies find that synaptic scaling is mediated by GluA2-lacking calcium receptors (CP-AMPARs), whereas others have found that scaling is mediated by GluA2-containing calcium-impermeable receptors (CI-AMPARs). Spontaneous network activity is observed in most developing circuits, and in the spinal cord this activity drives embryonic movements. Blocking spontaneous network activity in the chick embryo by infusing lidocaine in vivo triggers synaptic scaling in spinal motoneurons; here we show that AMPAergic scaling occurs through increases in mEPSC conductance that appear to be mediated by the insertion of GluA2-lacking AMPA receptors at the expense of GluA2-containing receptors. We have previously reported that in vivo blockade of GABAA transmission, at a developmental stage when GABA is excitatory, also triggered AMPAergic synaptic scaling. Here, we show that this form of AMPAergic scaling is also mediated by CP-AMPARs. These findings suggest that AMPAergic scaling triggered by blocking spiking activity or GABAA receptor transmission represents similar phenomena, supporting the idea that activity blockade triggers scaling by reducing GABAA transmission.
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Registered trials
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.