The role of GABAergic inhibition in ocular dominance plasticity
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During the last decade, we have gained much insight into the mechanisms that open and close a sensitive period of plasticity in the visual cortex. This brings the hope that novel treatments can be developed for brain injuries requiring renewed plasticity potential and neurodevelopmental brain disorders caused by defective synaptic plasticity. One of the central mechanisms responsible for opening the sensitive period is the maturation of inhibitory innervation. Many molecular and cellular events have been identified that drive this developmental process, including signaling through BDNF and IGF-1, transcriptional control by OTX2, maturation of the extracellular matrix, and GABA-regulated inhibitory synapse formation. The mechanisms through which the development of inhibitory innervation triggers and potentially closes the sensitive period may involve plasticity of inhibitory inputs or permissive regulation of excitatory synapse plasticity. Here, we discuss the current state of knowledge in the field and open questions to be addressed.
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Increasing inhibition from PV+ interneurons is implicated in regulating sensitive period plasticity in primary sensory cortices.
“Increasing inhibition from PV+ interneurons is implicated in regulating sensitive period plasticity in primary sensory cortices (Davis et al., 2015; Heimel et al., 2011; Hensch, 2005; Le Magueresse and Monyer, 2013; Werker and Hensch, 2015).”
From Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex? (2017) · cites this paper as Heimel et al., 2011
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- Authors
- Heimel, J. A., van Versendaal, D., & Levelt, C. N.
- Affiliations
- Netherlands Institute for Neuroscience (NL)
- Department of Molecular Visual Plasticity, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105BA Amsterdam, The Netherlands
- Corresponding author
- Levelt, Christiaan N.
- Venue
- Neural Plasticity
- Publisher
- Wiley
- Published
- 2011
- Volume
- 2011
- Pages
- 1-11
- ISSN
- 1687-5443 (ISSN-L)
- 2090-5904
- PMC
- PMC3150150
- OpenAlex
- W2155688542
- Cited by
- 57
- References
- 96
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 8 · 2015: 4 · 2014: 6 · 2013: 6 · 2012: 4
- FWCI
- 0.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Neural Plasticity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- KNAW Research Portal (The Royal Netherlands Academy of Arts and Sciences) (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- European Commission (223326)
- 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
- GABAergic inhibition, ocular dominance plasticity, visual cortex, sensitive period, brain-derived neurotrophic factor, insulin-like growth factor I, Otx2, extracellular matrix, inhibitory synapse formation, neurodevelopmental disorders, brain injury
- MeSH terms
- Animals, Cerebral Cortex, gamma-Aminobutyric Acid, Homeostasis, Humans, Interneurons, Neuronal Plasticity, Parvalbumins, Synapses, Visual Cortex, Excitatory Amino Acid Antagonists, Dominance, Ocular
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