Cited by 1,533Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionGenetics and Neurodevelopmental Disorders

The self-tuning neuron: synaptic scaling of excitatory synapses

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Turrigiano, Gina G.·2008·Cell

Abstract

Homeostatic synaptic scaling is a form of synaptic plasticity that adjusts the strength of all of a neuron's excitatory synapses up or down to stabilize firing. Current evidence suggests that neurons detect changes in their own firing rates through a set of calcium-dependent sensors that then regulate receptor trafficking to increase or decrease the accumulation of glutamate receptors at synaptic sites. Additional mechanisms may allow local or network-wide changes in activity to be sensed through parallel pathways, generating a nested set of homeostatic mechanisms that operate over different temporal and spatial scales.

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Crossref · 10.1016/j.cell.2008.10.008

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  • The existence of LTD avoids the problem of saturation, which could be essential for a mnemonic device.

    “The existence of LTD avoids the problem of saturation, which could be essential for a mnemonic device (366–371).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [368]

    In “The Stability Problem” (page unavailable), the paper groups LTP and LTD as learning-related plasticity mechanisms, then says such mechanisms can create destabilizing feedback that drives neuronal activity to saturation. It says nervous systems need other plasticity mechanisms to counteract those forces; it does not say that the existence of LTD avoids saturation. (LLM, conf=0.86)

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  • The firing rate set point is an emergent property that represents the stable point of all the opposing signaling pathways that operate on synaptic strength.

    “One interesting implication of this model is that the firing rate set point is an emergent property that represents the stable point of all the opposing signaling pathways that operate on synaptic strength (Turrigiano 2008).”

    From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Turrigiano 2008

    In Concluding Remarks, the paper proposes that the activity set point could arise where opposing forces regulating receptor accumulation equalize. The citing sentence presents this proposed model as fact and extends it to all opposing signaling pathways that affect synaptic strength, which the passage does not establish. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • If the contribution of CaMKII to synaptic transmission were a net gain that simply adds onto the preexisting excitatory drive of the cell, the system would be unstable and quickly saturate.

    “If this were the case, it has been argued that the system would be unstable and quickly saturate (366–371).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [368]

    In “The Stability Problem” (page not provided), the paper argues that unconstrained strengthening of excitatory synapses creates positive feedback that can drive neuronal activity to saturation. It does not make that argument specifically about a net additive contribution from CaMKII; its discussion of CaMKII in “Signaling Pathways Underlying Synaptic Scaling” concerns different homeostatic effects. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Synaptic scaling involves postsynaptic changes in receptor accumulation.

    “It is widely agreed that synaptic scaling involves postsynaptic changes in receptor accumulation (Turrigiano 2008), but under some circumstances additional presynaptic changes can also be recruited (Davis and Bezprozvanny 2001;Rich and Wenner 2007;Thiagarajan et al. 2007).”
  • Homeostasis occurs on a slower timescale of many hours or days; the cell senses excess activity and through a cellwide mechanism scales down all synapses in a multiplicative manner to restore excitatory drive to a set point.

    “The third mechanism, homeostasis, occurs on a slower timescale of many hours or days (368). In this case the cell senses the excess level of activity and through a cellwide mechanism scales down all synapses in a multiplicative manner to restore excitatory drive to a set point.”

    From Synaptic memory and CaMKII (2023) · cites this paper as [368]

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Authors
Turrigiano, G. G.
Affiliations
Brandeis University (US)
Corresponding author
Turrigiano, Gina G.
Venue
Cell
Publisher
Elsevier BV
Published
2008-10
Volume
135
Issue
3
Pages
422-435
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2047535883
Cited by
1,533
References
100
Citations by year
2026: 65 · 2025: 107 · 2024: 66 · 2023: 71 · 2022: 69 · 2021: 114 · 2020: 82 · 2019: 96 · 2018: 75 · 2017: 99 · 2016: 73 · 2015: 85 · 2014: 93 · 2013: 116 · 2012: 96
FWCI
5.82
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • Goddard Space Flight Center
  • National Eye Institute (EY14439, R01EY014439)
  • National Institute of Neurological Disorders and Stroke (NS 36853, R56NS036853, R01NS036853)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
homeostatic synaptic scaling, excitatory synapses, synaptic plasticity, neuronal firing rate, glutamate receptor trafficking, synaptic homeostasis
MeSH terms
Animals, Brain, Homeostasis, Humans, Neuronal Plasticity, Neurons, Synapses

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