ArticleProceedings of the National Academy of Sciences of the United States of America2012
Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed.
- TNF-dependent regulation of synaptic plasticity and neuronal activity: implications for psychiatric disorders.Molecular psychiatry · 2026Review
- Ethological learning during the critical period resets synaptic setpoints in mouse binocular visual cortex.Neuron · 2026Article
- TNF-α Deficiency Reduces Parvalbumin Neuron Density, Impairs Homeostatic Plasticity, Disrupts Synaptic Excitation-Inhibition Balance, and Prevents Critical Period Closure in the Auditory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Non-Synaptic Mechanism of Ocular Dominance Plasticity.ASN neuro · 2026Article
- Interactions between excitatory neurons and parvalbumin interneurons in V1 underlie neural mechanisms of amblyopia and visual stimulation treatment.Communications biology · 2024Article
- 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
- Chronic modulation of cAMP signaling elicits synaptic scaling irrespective of activity.iScience · 2024Article
- Astrocytes Are the Source of TNF Mediating Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Single-cell synaptome mapping: its technical basis and applications in critical period plasticity research.Frontiers in neural circuits · 2024Review
- Longitudinal development of the human white matter structural connectome and its association with brain transcriptomic and cellular architecture.Communications biology · 2023Article
- Age-related dysregulation of homeostatic control in neuronal microcircuits.Nature neuroscience · 2023Article
- Experience dependent plasticity of higher visual cortical areas in the mouse.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Thalamic regulation of a visual critical period and motor behavior.Cell reports · 2023Article
- Enriched binocular experience followed by sleep optimally restores binocular visual cortical responses in a mouse model of amblyopia.Communications biology · 2023Article
- Cortical feedback modulates distinct critical period development in mouse visual thalamus.iScience · 2023Article
- Differentiation of Hebbian and homeostatic plasticity mechanisms within layer 5 visual cortex neurons.Cell reports · 2022Article
- Optimizing intact skull intrinsic signal imaging for subsequent targeted electrophysiology across mouse visual cortex.Scientific reports · 2022Article
- Homeostatic regulation of extracellular signal-regulated kinase 1/2 activity and axonal KFrontiers in cellular neuroscience · 2022Article
- Long-Term Environmental Enrichment Relieves Dysfunctional Cognition and Synaptic Protein Levels Induced by Prenatal Inflammation in Older CD-1 Mice.Neural plasticity · 2022Article
22 more citing papers are in PubMed but not listed here.
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4 authors.
Funding
Abstract
Ocular dominance (OD) plasticity in the visual cortex is a classic model system for understanding developmental plasticity, but the visual cortex also shows plasticity in adulthood. Whether the plasticity mechanisms are similar or different at the two ages is not clear. Several plasticity mechanisms operate during development, including homeostatic plasticity, which acts to maintain the total excitatory drive to a neuron. In agreement with this idea, we found that an often-studied substrain of C57BL/6 mice, C57BL/6JOlaHsd (6JOla), lacks both the homeostatic component of OD plasticity as assessed by intrinsic signal imaging and synaptic scaling of mEPSC amplitudes after a short period of dark exposure during the critical period, whereas another substrain, C57BL/6J (6J), exhibits both plasticity processes. However, in adult mice, OD plasticity was identical in the 6JOla and 6J substrains, suggesting that adult plasticity occurs by a different mechanism. Consistent with this interpretation, adult OD plasticity was normal in TNFα knockout mice, which are known to lack juvenile synaptic scaling and the homeostatic component of OD plasticity, but was absent in adult α-calcium/calmodulin-dependent protein kinase II;T286A (αCaMKII(T286A)) mice, which have a point mutation that prevents autophosphorylation of αCaMKII. We conclude that increased responsiveness to open-eye stimulation after monocular deprivation during the critical period is a homeostatic process that depends mechanistically on synaptic scaling during the critical period, whereas in adult mice it is mediated by a different mechanism that requires αCaMKII autophosphorylation. Thus, our study reveals a transition between homeostatic and long-term potentiation-like plasticity mechanisms with increasing age.
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