ArticleScience advances2025
LARGE protein drives activity-induced homeostatic resetting.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the brain, memory can be coded as relative differences in synaptic strength produced by Hebbian plasticity [e.g., long-term potentiation (LTP)]. However, changes in neuronal activity, including the saturation of synaptic strength by the positive-feedback nature of Hebbian plasticity, could deteriorate the encoded memory. Homeostatic plasticity is thought to contribute to the stability of the encoded memory by maintaining the relative differences in synaptic strength against persistent destabilizing changes in neuronal activity. However, it remains unclear how and when these two types of plasticity work together in the context of memory. Here, we have demonstrated that LARGE, a protein associated with intellectual disability, drives homeostatic resetting several hours after LTP by down-regulating AMPA-receptor trafficking via the Golgi apparatus. LARGE deficiency impairs long-term memory formation in mice. Our study reveals a potential molecular mechanism underlying the stability of memory mediated by cross-talk between Hebbian and homeostatic plasticity.
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