ArticleThe Journal of physiology2025
Intersectin-1 enhances calcium-dependent replenishment of the readily releasable pool of synaptic vesicles during development.
Article in The Journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Munc13-1 couples DAG and CaScience advances · 2026Article
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Input-Specific Organization of Intrinsic Excitability Expands Coding Capacity of Fast-Spiking Auditory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Intersectin and endophilin condensates prime synaptic vesicles for release site replenishment.Nature neuroscience · 2025Article
- CircITSN1/EIF4A3/Itsn1 axis mediates postoperative cognitive dysfunction in aged mice: A novel mechanism and therapeutic target.Molecular therapy. Nucleic acids · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Intersectin-1 (Itsn1) is a scaffold protein that plays a key role in coupling exocytosis and endocytosis of synaptic vesicles (SVs). However, it is unclear whether and how Itsn1 regulates these processes to support efficient neurotransmission during development. To address this, we examined the calyx of Held synapse in the auditory brainstem of wild-type and Itsn1 mutant mice before (immature) and after (mature) the onset of hearing. Itsn1 was present in the pre- and postsynaptic compartments at both developmental stages. Loss of function of Itsn1 did not alter presynaptic action potentials, Ca
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