ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Disruption of NMDAR Function Prevents Normal Experience-Dependent Homeostatic Synaptic Plasticity in Mouse Primary Visual Cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Characterizing Spatial Associations Between GluCEST MRI and Neurotransmitter Receptor Density in the Human Cortex.Human brain mapping · 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
- Inhibition of FLT1 Attenuates Neurodevelopmental Abnormalities and Cognitive Impairment in Offspring Caused by Maternal Prenatal Stress.Applied biochemistry and biotechnology · 2024Article
- Central amygdala CRF+ neurons promote heightened threat reactivity following early life adversity in mice.Nature communications · 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
- Loss of Depalmitoylation Disrupts Homeostatic Plasticity of AMPARs in a Mouse Model of Infantile Neuronal Ceroid Lipofuscinosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The effect of ketamine on synaptic mistuning induced by impaired glutamate reuptake.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Differentiation of Hebbian and homeostatic plasticity mechanisms within layer 5 visual cortex neurons.Cell reports · 2022Article
- NMDA receptors in visual cortex are necessary for normal visuomotor integration and skill learning.eLife · 2022Article
- Metaplasticity framework for cross-modal synaptic plasticity in adults.Frontiers in synaptic neuroscience · 2022Review
- Aberrant maturation and connectivity of prefrontal cortex in schizophrenia-contribution of NMDA receptor development and hypofunction.Molecular psychiatry · 2022Review
- The Shaping of AMPA Receptor Surface Distribution by Neuronal Activity.Frontiers in synaptic neuroscience · 2022Review
- Hyperexcitability and Homeostasis in Fragile X Syndrome.Frontiers in molecular neuroscience · 2021Article
- Naturalistic Spike Trains Drive State-Dependent Homeostatic Plasticity in Superficial Layers of Visual Cortex.Frontiers in synaptic neuroscience · 2021Article
- Cortical and Subcortical Circuits for Cross-Modal Plasticity Induced by Loss of Vision.Frontiers in neural circuits · 2021Article
- Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Mechanisms of Homeostatic Synaptic PlasticityFrontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Homeostatic regulation of synaptic strength allows for maintenance of neural activity within a dynamic range for proper circuit function. There are largely two distinct modes of synaptic plasticity that allow for homeostatic adaptation of cortical circuits: synaptic scaling and sliding threshold (BCM theory). Previous findings suggest that the induction of synaptic scaling is not prevented by blocking NMDARs, whereas the sliding threshold model posits that the synaptic modification threshold of LTP and LTD readjusts with activity and thus the outcome of synaptic plasticity is NMDAR dependent. Although synaptic scaling and sliding threshold have been considered two distinct mechanisms, there are indications from recent studies that these two modes of homeostatic plasticity may interact or that they may operate under two distinct activity regimes. Here, we report using both sexes of mouse that acute genetic knock-out of the obligatory subunit of NMDAR or acute pharmacological block of NMDAR prevents experience-dependent homeostatic regulation of AMPAR-mediated miniature EPSCs in layer 2/3 of visual cortex. This was not due to gross changes in postsynaptic neuronal activity with inhibiting NMDAR function as determine by c-Fos expression and two-photon Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.