ArticleCell reports2024
A dendritic mechanism for balancing synaptic flexibility and stability.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Domain-specific schema reuse supports flexible learning to learn in the primate brain.Nature communications · 2026Article
- Plateau potentials are instructive signals for behavioral timescale synaptic plasticity in the neocortex.bioRxiv : the preprint server for biology · 2025Article
- Comparative transcriptomics reveals shifts in cortical architecture at the metatherian/eutherian transition.bioRxiv : the preprint server for biology · 2025Article
- A Critical Look at Critical Periods.Annual review of vision science · 2025Review
- Learning to combine top-down context and feed-forward representations under ambiguity with apical and basal dendrites.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Distinct synaptic plasticity rules operate across dendritic compartments in vivo during learning.Science (New York, N.Y.) · 2025Article
- Structure-function relationships across scales: implications for atlases.Frontiers in neuroscience · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Biological and artificial neural networks learn by modifying synaptic weights, but it is unclear how these systems retain previous knowledge and also acquire new information. Here, we show that cortical pyramidal neurons can solve this plasticity-versus-stability dilemma by differentially regulating synaptic plasticity at distinct dendritic compartments. Oblique dendrites of adult mouse layer 5 cortical pyramidal neurons selectively receive monosynaptic thalamic input, integrate linearly, and lack burst-timing synaptic potentiation. In contrast, basal dendrites, which do not receive thalamic input, exhibit conventional NMDA receptor (NMDAR)-mediated supralinear integration and synaptic potentiation. Congruently, spiny synapses on oblique branches show decreased structural plasticity in vivo. The selective decline in NMDAR activity and expression at synapses on oblique dendrites is controlled by a critical period of visual experience. Our results demonstrate a biological mechanism for how single neurons can safeguard a set of inputs from ongoing plasticity by altering synaptic properties at distinct dendritic domains.
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Registered trials
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