Inhibitory threshold for critical-period activation in primary visual cortex
Abstract
Neuronal circuits across several systems display remarkable plasticity to sensory input during postnatal development. Experience-dependent refinements are often restricted to well-defined critical periods in early life, but how these are established remains mostly unknown. A representative example is the loss of responsiveness in neocortex to an eye deprived of vision. Here we show that the potential for plasticity is retained throughout life until an inhibitory threshold is attained. In mice of all ages lacking an isoform of GABA (gamma-aminobutyric acid) synthetic enzyme (GAD65), as well as in immature wild-type animals before the onset of their natural critical period, benzodiazepines selectively reduced a prolonged discharge phenotype to unmask plasticity. Enhancing GABA-mediated transmission early in life rendered mutant animals insensitive to monocular deprivation as adults, similar to normal wild-type mice. Short-term presynaptic dynamics reflected a synaptic reorganization in GAD65 knockout mice after chronic diazepam treatment. A threshold level of inhibition within the visual cortex may thus trigger, once in life, an experience-dependent critical period for circuit consolidation, which may otherwise lie dormant.
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A precocious increase of GABA transmission in V1 and precocious maturation of PV cells trigger an earlier onset of the critical period, whereas an accelerated rise of PNNs results in earlier closure.
“A precocious increase of GABA transmission in V1 and precocious maturation of PV cells trigger an earlier onset (18,41), whereas an accelerated rise of PNNs results in an earlier closure of the critical period (27).”
From MeCP2 regulates the timing of critical period plasticity that shapes functional connectivity in primary visual cortex (2015) · cites this paper as [41]
Disruption of excitatory-inhibitory balance shifts the timing and quality of critical period development in primary visual cortex.
“Accordingly, disruption of E-I balance powerfully shifts the timing and quality of critical period development, as seen in the primary visual cortex (V1) (27–29).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [28]
In transgenic mice with disrupted GABA synthesis at synaptic terminals, the critical period for MD sensitivity fails to open unless GABA agonists are applied.
“In transgenic mice with disrupted GABA synthesis at synaptic terminals, the critical period for MD sensitivity fails to open unless GABA agonists are applied (308, 482).”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [308]
Maturation of inhibitory circuits, in particular mediated by PVBCs, is necessary for the expression of early competitive plasticity.
“the maturation of inhibitory circuits, in particular mediated by PVBCs, is necessary for the expression of this early competitive plasticity”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [308]
Postnatal maturation of cortical inhibitory networks is needed to start the critical period.
“The maturation of cortical inhibitory networks in the postnatal brain is important for initiating this critical period (Fagiolini and Hensch, 2000; Sugiyama et al., 2008).”
From Clock Genes Control Cortical Critical Period Timing (2015) · cites this paper as Fagiolini and Hensch, 2000
A 10-day diazepam treatment from P23 to P33 prevented later adult plasticity in Clock-mutant mice.
“Moreover, mimicking a critical period by 10-day injection (P23–P33) of diazepam (Fagiolini and Hensch, 2000) prevented later adult plasticity in Clock−/− mice (Figure 3C).”
From Clock Genes Control Cortical Critical Period Timing (2015) · cites this paper as Fagiolini and Hensch, 2000
VEP recordings were performed using standard techniques in mice.
“VEPs were recorded under nembutal/chlorprothixene anesthesia using standard techniques in mice (Fagiolini and Hensch, 2000; Porciatti et al., 1999).”
From Clock Genes Control Cortical Critical Period Timing (2015) · cites this paper as Fagiolini and Hensch, 2000
Excitatory-inhibitory balance is crucial for correct development of visual function during the critical period, suggesting that spine maturation and plasticity are important underlying components of functional changes in the visual pathway.
“This in line with previous findings that found that excitatory-inhibitory balance is crucial for correct development of visual function during the critical period [45], thus suggesting that spine maturation and plasticity is an important underlying component of the functional changes that occur in the visual pathway.”
From Experience-dependent structural plasticity in the cortex (2011) · cites this paper as [45]
Gene-targeted deletion of the GABAergic synthetic enzyme GAD65 in mice abolishes developmental plasticity.
“Gene-targeted deletion of the GABAergic synthetic enzyme GAD65 in mice abolishes developmental plasticity”
From Neuronal Dynamics and Neuropsychiatric Disorders: Toward a Translational Paradigm for Dysfunctional Large-Scale Networks (2012) · cites this paper as Fagiolini and Hensch, 2000
This loss can be rescued at any age with benzodiazepines.
“this loss can be rescued at any age with benzodiazepines”
From Neuronal Dynamics and Neuropsychiatric Disorders: Toward a Translational Paradigm for Dysfunctional Large-Scale Networks (2012) · cites this paper as Fagiolini and Hensch, 2000
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Perineuronal Nets Play a Role in Regulating Striatal Function in the Mouse
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Brief dark exposure restored ocular dominance plasticity in aging mice and after a cortical stroke
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Enhancement of visual cortex plasticity by dark exposure
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Serotonergic neuromodulation of synaptic plasticity
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- Authors
- Fagiolini, M., & Hensch, T. K.
- Affiliations
- RIKEN (JP)
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Hensch, Takao K.
- ORCID
- Fagiolini, Michela
- Venue
- Nature
- Published
- 2000-03
- Volume
- 404
- Issue
- 6774
- Pages
- 183-186
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1994124070
- Cited by
- 716
- References
- 30
- Citations by year
- 2026: 22 · 2025: 37 · 2024: 30 · 2023: 30 · 2022: 25 · 2021: 29 · 2020: 33 · 2019: 29 · 2018: 31 · 2017: 26 · 2016: 26 · 2015: 37 · 2014: 38 · 2013: 42 · 2012: 36
- FWCI
- 7.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Science Foundation
- 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 › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- critical period, primary visual cortex, monocular deprivation, GABA synthesis, benzodiazepines, diazepam, synaptic plasticity, experience-dependent plasticity, GABAergic inhibition
- MeSH terms
- Aging, Animals, Haplorhini, Critical Period, Psychological, Diazepam, gamma-Aminobutyric Acid, Mice, Inbred C57BL, Neuronal Plasticity, Sensory Deprivation, Visual Cortex, Visual Perception, Mice, Knockout, Mice
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