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Cited by 99Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeural dynamics and brain function

LTP and adaptation to inactivity: Overlapping mechanisms and implications for metaplasticity

Thiagarajan, Tara C., Lindskog, Maria, Malgaroli, Antonio, Tsien, Richard W.·2007·Neuropharmacology
DOI 10.1016/j.neuropharm.2006.07.030
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Abstract

LTP and other rapidly induced forms of synaptic modification tune individual synaptic weights, whereas slower forms of plasticity such as adaptation to inactivity are thought to keep neurons within their firing limits and preserve their capability for information processing. Here we describe progress in understanding the relationship between LTP and adaptation to inactivity. A prevailing view is that adaptation to inactivity is purely postsynaptic, scales synaptic strength uniformly across all synapses, and thus preserves relative synaptic weights without interfering with signatures of prior LTP or the relative capacity for future LTP. However, recent evidence in hippocampal neurons indicates that, like LTP, adaptation to AMPA receptor blockade can draw upon a repertoire of synaptic expression mechanisms including enhancement of presynaptic vesicular turnover and increased quantal amplitude mediated by recruitment of homomeric GluR1 AMPA receptors. These pre- and postsynaptic changes appeared coordinated and preferentially expressed at subset of synapses, thereby increasing the variability of miniature EPSCs. In contrast to the NMDA receptor-, Ca2+ entry-dependent induction of LTP, adaptation to inactivity may be mediated by attenuation of voltage-sensitive L-type Ca2+ channel function. The associated intracellular signaling involves elevation of betaCaMKII, which in turn downregulates alphaCaMKII, a key player in LTP. Thus, adaptation to inactivity and LTP are not strictly i…

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  • Under some circumstances, additional presynaptic changes can be recruited during synaptic scaling.

    “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).”

    From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Thiagarajan et al. 2007

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Authors
Thiagarajan, T. C., Lindskog, M., Malgaroli, A., & Tsien, R. W.
Affiliations
  • Stanford Medicine (US)
  • Vita-Salute San Raffaele University (IT)
Corresponding author
Tsien, Richard W.
ORCID
Venue
Neuropharmacology
Publisher
Elsevier BV
Published
2007-01
Volume
52
Issue
1
Pages
156-175
ISSN
0028-3908 (ISSN-L)
DOI
10.1016/j.neuropharm.2006.07.030
OpenAlex
W2020449445
Cited by
99
References
13
Citations by year
2024: 4 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 6 · 2013: 9 · 2012: 7
FWCI
0.71
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuropharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
long-term potentiation, metaplasticity, synaptic plasticity, AMPA receptor blockade, miniature EPSCs, L-type calcium channels, CaMKIIα, hippocampal neurons
MeSH terms
Adaptation, Biological, Animals, Electric Stimulation, Synaptic Transmission, Synapses, Receptors, Glutamate, Long-Term Potentiation

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