ArticleProceedings of the National Academy of Sciences of the United States of America2021
All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Binocular Circuitry as a Model for Understanding Experience-Dependent Circuit Development across the Mammalian Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Rapid plasticity of default-mode local network architectures following adult-onset blindness.Cell reports · 2026Article
- Tuning excitatory input to fast-spiking parvalbumin-positive interneurons: a lever for plasticity and hyperexcitability across the lifespan.Frontiers in synaptic neuroscience · 2026Article
- Genetic Mechanisms of Experience-Dependent Neuronal Plasticity.Annual review of genetics · 2025Review
- Transcriptomic and protein analysis of human cortex reveals genes and pathways linked to NPTX2 disruption in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Targeting interleukin-2-inducible T cell kinase ameliorates immune-mediated aplastic anemia.Cancer immunology, immunotherapy : CII · 2025Article
- Excitatory/Inhibitory imbalance as a mechanism linking autism and sleep problems.Current opinion in neurobiology · 2025Review
- Developmental properties of parvalbumin-positive gamma-aminobutyric acid interneurons and the effect of fluoxetine treatment and binocular form deprivation on them in the visual cortex of adult rats.International journal of ophthalmology · 2025Article
- Blockade of GluN2B-Containing NMDA Receptors Prevents Potentiation and Depression of Responses during Ocular Dominance Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Activation AMPK in Hypothalamic Paraventricular Nucleus Improves Renovascular Hypertension Through ERK1/2-NF-κB Pathway.Cardiovascular toxicology · 2024Article
- Sleep restores an optimal computational regime in cortical networks.Nature neuroscience · 2024Article
- Selective plasticity of fast and slow excitatory synapses on somatostatin interneurons in adult visual cortex.Nature communications · 2023Article
- The neuronal pentraxin Nptx2 regulates complement activity and restrains microglia-mediated synapse loss in neurodegeneration.Science translational medicine · 2023Article
- Visual Cortical Plasticity: Molecular Mechanisms as Revealed by Induction Paradigms in Rodents.International journal of molecular sciences · 2023Review
- Parvalbumin-Positive Interneurons Regulate Cortical Sensory Plasticity in Adulthood and Development Through Shared Mechanisms.Frontiers in neural circuits · 2022Review
- A biomarker-authenticated model of schizophrenia implicating NPTX2 loss of function.Science advances · 2021Article
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15 authors.
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Abstract
Disinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience. Our investigation on disinhibitory mechanisms in the classical model of ocular dominance plasticity uncovered an unexpected form of experience-dependent circuit plasticity. In the layer 2/3 of mouse visual cortex, monocular deprivation triggers a complete, "all-or-none," elimination of connections from pyramidal cells onto nearby parvalbumin-positive interneurons (Pyr→PV). This binary form of circuit plasticity is unique, as it is transient, local, and discrete. It lasts only 1 d, and it does not manifest as widespread changes in synaptic strength; rather, only about half of local connections are lost, and the remaining ones are not affected in strength. Mechanistically, the deprivation-induced loss of Pyr→PV is contingent on a reduction of the protein neuropentraxin2. Functionally, the loss of Pyr→PV is absolutely necessary for ocular dominance plasticity, a canonical model of deprivation-induced model of cortical remodeling. We surmise, therefore, that this all-or-none loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.
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