ArticleThe Journal of cell biology2021
Endophilin A1 drives acute structural plasticity of dendritic spines in response to Ca2+/calmodulin.
Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Signaling Pathways in Depression and Neuroinflammation: Focus on New Pathophysiological Proteins and Therapeutic Compounds.Antioxidants (Basel, Switzerland) · 2026Review
- Overexpression of Synaptopodin increases the number of spine apparatuses and active synapses of dentate granule cells.Scientific reports · 2026Article
- Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Progressive reduction of nuclear receptor Nr4a1 mediates age-dependent cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Inflammatory Factor IL1α Induces Aberrant Astrocyte Proliferation in Spinal Cord Injury Through the Grin2c/CaNeuroscience bulletin · 2024Article
- Synaptic plasticity in schizophrenia pathophysiology.IBRO neuroscience reports · 2023Article
- Article
- The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson's Disease Model Mice.Journal of Parkinson's disease · 2023Article
- Synaptic plasticity in schizophrenia pathophysiology.IBRO neuroscience reports · 2022Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of long-term potentiation (LTP) in excitatory neurons triggers a large transient increase in the volume of dendritic spines followed by decays to sustained size expansion, a process termed structural LTP (sLTP) that contributes to the cellular basis of learning and memory. Although mechanisms regulating the early and sustained phases of sLTP have been studied intensively, how the acute spine enlargement immediately after LTP stimulation is achieved remains elusive. Here, we report that endophilin A1 orchestrates membrane dynamics with actin polymerization to initiate spine enlargement in NMDAR-mediated LTP. Upon LTP induction, Ca2+/calmodulin enhances binding of endophilin A1 to both membrane and p140Cap, a cytoskeletal regulator. Consequently, endophilin A1 rapidly localizes to the plasma membrane and recruits p140Cap to promote local actin polymerization, leading to spine head expansion. Moreover, its molecular functions in activity-induced rapid spine growth are required for LTP and long-term memory. Thus, endophilin A1 serves as a calmodulin effector to drive acute structural plasticity necessary for learning and memory.
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Registered trials
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