Rapid Synaptic Scaling Induced by Changes in Postsynaptic Firing
Open accessAbstract
Homeostatic synaptic scaling adjusts a neuron's excitatory synaptic strengths up or down to compensate for perturbations in activity. Little is known about the molecular pathway(s) involved, nor is it clear which aspect of "activity"-local synaptic signaling, postsynaptic firing, or large-scale changes in network activity-is required to induce synaptic scaling. Here, we selectively block either postsynaptic firing in individual neurons or a fraction of presynaptic inputs, while optically monitoring changes in synaptic strength. We find that synaptic scaling is rapidly induced by block of postsynaptic firing, but not by local synaptic blockade, and is mediated through a drop in somatic calcium influx, reduced activation of CaMKIV, and an increase in transcription. Cortical neurons thus homeostatically adjust synaptic strengths in response to changes in their own firing rate, a mechanism with the computational advantage of efficiently normalizing synaptic strengths without interfering with synapse-specific mechanisms of information storage.
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Three other studies failed to observe local enhancement of AMPAR accumulation at inactivated synapses.
“In contrast, three other studies failed to observe such a local enhancement of AMPAR accumulation at inactivated synapses.”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Ibata et al. 2008
Selectively blocking postsynaptic firing in neocortical neurons scales synapses up through a process that requires a drop in somatic calcium influx, reduced activation of CaMKIV, and transcription.
“Selectively blocking postsynaptic firing in neocortical neurons scales synapses up through a process that requires a drop in somatic calcium influx, reduced activation of CaMKIV, and transcription (Ibata et al. 2008).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Ibata et al. 2008
Selectively blocking firing by microperfusion of TTX to the soma of individual neurons scales up synaptic strengths to the same degree as blockade of network activity, whereas local block of synaptic transmission does not induce a local enhancement of receptor accumulation.
“Selectively blocking firing by microperfusion of TTX to the soma of individual neurons scales up synaptic strengths to the same degree as blockade of network activity, whereas local block of synaptic transmission does not induce a local enhancement of receptor accumulation (Ibata et al. 2008).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Ibata et al. 2008
There is strong evidence that synaptic scaling is a cell-autonomous process induced by changes in a neuron's own firing.
“there is strong evidence that synaptic scaling is a cell-autonomous process induced by changes in a neuron's own firing.”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Ibata et al. 2008
Scaling is a gradual and cumulative process evident after as little as 4-6 h of activity blockade.
“Inconsistent with the above model is the observation that scaling is a gradual and cumulative process evident after as little as 4-6 h of activity blockade (Sutton et al. 2006;Ibata et al. 2008), whereas TNFa-dependent scaling was only observed after prolonged activity block (48 h) (Stellwagen and Malenka 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Ibata et al. 2008
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References 48 · Cited by 446
- Authors
- Ibata, K., Sun, Q., & Turrigiano, G. G.
- Affiliations
- Brandeis University (US)
- Corresponding author
- Turrigiano, Gina G.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2008-03
- Volume
- 57
- Issue
- 6
- Pages
- 819-826
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2168976498
- Cited by
- 446
- References
- 48
- Citations by year
- 2026: 8 · 2025: 25 · 2024: 22 · 2023: 20 · 2022: 31 · 2021: 19 · 2020: 36 · 2019: 23 · 2018: 22 · 2017: 30 · 2016: 28 · 2015: 19 · 2014: 21 · 2013: 35 · 2012: 24
- FWCI
- 11.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2000 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (IBN 023519)
- National Institutes of Health (NS 36853)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- synaptic scaling, homeostatic plasticity, synaptic efficacy, CaMKIV, transcription, cortical neurons, synaptic plasticity, firing rate
- MeSH terms
- Anesthetics, Local, Animals, Animals, Newborn, Bacterial Proteins, Brain, Calcium, Hydrogen-Ion Concentration, Luminescent Proteins, Synaptic Transmission, Neurons, Nickel, Quinoxalines, Synapses, Tetrodotoxin, Time Factors, Transfection, Valine, Receptors, AMPA, Excitatory Amino Acid Antagonists, Rats, Long-Evans, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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