ArticleCerebral cortex (New York, N.Y. : 1991)2009
Double dissociation of spike timing-dependent potentiation and depression by subunit-preferring NMDA receptor antagonists in mouse barrel cortex.
Article in Cerebral cortex (New York, N.Y. : 1991), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 139 citations in OpenAlex.
- Article
- Coincidence detection between apical and basal dendrites drives STDP in cerebellar Golgi cells.Communications biology · 2025Article
- Neuronal traveling waves form preferred pathways using synaptic plasticity.Journal of computational neuroscience · 2025Article
- Inhibitory maturation and ocular dominance plasticity in mouse visual cortex require astrocyte CB1 receptors.iScience · 2024Article
- Developmental Spike Timing-Dependent Long-Term Depression Requires Astrocyte d-Serine at L2/3-L2/3 Synapses of the Mouse Somatosensory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Astrocytes mediate two forms of spike timing-dependent depression at entorhinal cortex-hippocampal synapses.eLife · 2024Article
- Aberrant activation of hippocampal astrocytes causes neuroinflammation and cognitive decline in mice.PLoS biology · 2024Article
- Variation and convergence in the morpho-functional properties of the mammalian neocortex.Frontiers in systems neuroscience · 2024Review
- GluN2A or GluN2B subunits of the NMDA receptor contribute to changes in neuronal excitability and impairments in LTP in the hippocampus of aging mice but do not mediate detrimental effects of oligomeric Aβ (1-42).Frontiers in aging neuroscience · 2024Article
- Timing to be precise? An overview of spike timing-dependent plasticity, brain rhythmicity, and glial cells interplay within neuronal circuits.Molecular psychiatry · 2023Review
- Role of Group I Metabotropic Glutamate Receptors in Spike Timing-Dependent Plasticity.International journal of molecular sciences · 2022Article
- Advances and Barriers in Understanding PresynapticFrontiers in molecular neuroscience · 2022Review
- Synaptic NMDA receptor activity at resting membrane potentials.Frontiers in cellular neuroscience · 2022Article
- Presynaptic NMDA Receptors Influence CaNeural plasticity · 2022Article
- Dopaminergic Neuromodulation of Spike Timing Dependent Plasticity in Mature Adult Rodent and Human Cortical Neurons.Frontiers in cellular neuroscience · 2021Article
- Calcium and Spike Timing-Dependent Plasticity.Frontiers in cellular neuroscience · 2021Review
- Synaptic Plasticity and Oscillations in Alzheimer's Disease: A Complex Picture of a Multifaceted Disease.Frontiers in molecular neuroscience · 2021Article
- Astrocyte-mediated spike-timing-dependent long-term depression modulates synaptic properties in the developing cortex.PLoS computational biology · 2020Article
- Astrocyte-mediated switch in spike timing-dependent plasticity during hippocampal development.Nature communications · 2020Article
- Structural basis of subtype-selective competitive antagonism for GluN2C/2D-containing NMDA receptors.Nature communications · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Spike timing-dependent plasticity (STDP) is a strong candidate for an N-methyl-D-aspartate (NMDA) receptor-dependent form of synaptic plasticity that could underlie the development of receptive field properties in sensory neocortices. Whilst induction of timing-dependent long-term potentiation (t-LTP) requires postsynaptic NMDA receptors, timing-dependent long-term depression (t-LTD) requires the activation of presynaptic NMDA receptors at layer 4-to-layer 2/3 synapses in barrel cortex. Here we investigated the developmental profile of t-LTD at layer 4-to-layer 2/3 synapses of mouse barrel cortex and studied their NMDA receptor subunit dependence. Timing-dependent LTD emerged in the first postnatal week, was present during the second week and disappeared in the adult, whereas t-LTP persisted in adulthood. An antagonist at GluN2C/D subunit-containing NMDA receptors blocked t-LTD but not t-LTP. Conversely, a GluN2A subunit-preferring antagonist blocked t-LTP but not t-LTD. The GluN2C/D subunit requirement for t-LTD appears to be synapse specific, as GluN2C/D antagonists did not block t-LTD at horizontal cross-columnar layer 2/3-to-layer 2/3 synapses, which was blocked by a GluN2B antagonist instead. These data demonstrate an NMDA receptor subunit-dependent double dissociation of t-LTD and t-LTP mechanisms at layer 4-to-layer 2/3 synapses, and suggest that t-LTD is mediated by distinct molecular mechanisms at different synapses on the same postsynaptic neuron.
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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.