Persistence of Experience-Induced Homeostatic Synaptic Plasticity through Adulthood in Superficial Layers of Mouse Visual Cortex
Open accessAbstract
It is well established that sensory cortices of animals can be modified by sensory experience, especially during a brief early critical period in development. Theoretical analyses indicate that there are two synaptic plasticity mechanisms required: input-specific synaptic modifications and global homeostatic mechanisms to provide stability to neural networks. Experience-dependent homeostatic synaptic plasticity mechanisms have subsequently been demonstrated in the visual cortex of juvenile animals. Here, we report that experience-dependent homeostatic synaptic plasticity persists through adulthood in the superficial layers of the mouse visual cortex. We found that 2 d of visual deprivation in the form of dark rearing is necessary and sufficient to cause an increase in AMPA receptor-mediated miniature EPSC amplitude in layer 2/3 neurons. This increase was rapidly reversed by 1 d of light exposure. This reversible change in synaptic strength persisted in adult mice past the critical period for ocular dominance plasticity, which is reported to end at approximately 1 month of age in rodents. Interestingly, the mechanism of homeostatic synaptic modifications in 3-month-old mice differed from that in young mice (3 weeks old) in that the multiplicative nature of synaptic scaling is lost. Our results demonstrate that the superficial layers of adult mouse visual cortex retain the ability to undergo reversible experience-dependent homeostatic synaptic plasticity.
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These two modes of deprivation may induce different forms of compensatory synaptic plasticity.
“In contrast, dark rearing increases the abundance of GluA2-lacking receptors and requires GluA1 phosphorylation, suggesting that these two modes of deprivation may induce different forms of compensatory synaptic plasticity (Goel and Lee 2007;Goel et al. 2011).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Goel and Lee 2007
The Results section reports that dark rearing increases AMPA receptor-mediated mEPSC amplitude, supporting compensatory synaptic plasticity. The Discussion describes possible differences between scaling synapses up and down, but does not compare the two modes of deprivation in the citing sentence or establish that they induce different forms of plasticity. (LLM, conf=0.79)
Experimental — accuracy not yet measuredDark rearing increases the abundance of GluA2-lacking receptors and requires GluA1 phosphorylation.
“In contrast, dark rearing increases the abundance of GluA2-lacking receptors and requires GluA1 phosphorylation, suggesting that these two modes of deprivation may induce different forms of compensatory synaptic plasticity (Goel and Lee 2007;Goel et al. 2011).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Goel and Lee 2007
The Results section (page unavailable) reports that two days of dark rearing increased AMPA receptor-mediated mEPSC amplitude in mouse visual cortex. The Discussion (page unavailable) says dark rearing increased GluR1 (GluA1) phosphorylation, but our copy does not establish that phosphorylation is required or that GluA2-lacking receptors become more abundant. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn visual cortex, expression of synaptic scaling is developmentally regulated: it is expressed by layer 4 pyramidal neurons early in postnatal development, then turns off in layer 4 and begins in layer 2/3 around the opening of the classical visual system critical period, persisting into adulthood.
“In visual cortex the expression of synaptic scaling is developmentally regulated (Desai et al. 2002;Maffei et al. 2004Maffei et al. , 2006;;Maffei and Turrigiano 2008); synaptic scaling is expressed by pyramidal neurons in layer 4 early in postnatal development, but then turns off in layer 4 and begins to be expressed in layer 2/3 pyramidal neurons around the opening of the classical visual system”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Goel and Lee 2007
The Discussion (page unavailable) reports scaling in layer 4 at P14–P16 but not P21–P23, with the opposite pattern in layer 2/3; it also says the authors’ data extend layer 2/3 plasticity through adulthood. Our copy does not establish that the switch coincides with the opening of the classical visual critical period, or identify the early layer 4 cells specifically as pyramidal neurons. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe same visual deprivation paradigm that scales minis up in younger mice produces nonmultiplicative changes in minis in older mice.
“This possibility is raised by the finding that the same visual deprivation paradigm that scales minis up in younger mice produces nonmultiplicative changes in minis in older mice, suggesting that not all synapses are affected equally (Goel and Lee 2007); however, this could also reflect the simultaneous activation of synaptic scaling and Hebbian, synapse-specific mechanisms (see Turrigiano 2011”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Goel and Lee 2007
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- Authors
- Goel, A., & Lee, H.-K.
- Affiliations
- University of Maryland, College Park (US)
- ORCID
- Lee, H.-K.
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-06-20
- Volume
- 27
- Issue
- 25
- Pages
- 6692-6700
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2601561
- OpenAlex
- W1985322212
- Cited by
- 251
- References
- 8
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 8 · 2023: 12 · 2022: 11 · 2021: 11 · 2020: 12 · 2019: 14 · 2018: 16 · 2017: 15 · 2016: 11 · 2015: 12 · 2014: 11 · 2013: 26 · 2012: 21
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (R01EY014882)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Visual perception and processing mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- homeostatic plasticity, experience-dependent plasticity, visual cortex, dark rearing, visual deprivation, AMPA receptors, miniature EPSCs, layer 2/3 neurons, synaptic scaling, critical period, ocular dominance, adult plasticity, mouse visual cortex
- MeSH terms
- Age Factors, Animals, Animals, Newborn, Darkness, Homeostasis, Mice, Inbred C57BL, Neuronal Plasticity, Sensory Deprivation, Visual Cortex, Visual Pathways, Mice
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