ArticleProceedings of the National Academy of Sciences of the United States of America2024
Different states of synaptic vesicle priming explain target cell type-dependent differences in neurotransmitter release.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 15 citations in OpenAlex.
- Alternative splicing of synaptotagmin 7 regulates oligomerization and short-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Selective, genetically induced increase in synaptic vesicle priming.Science advances · 2026Article
- Munc13-1 couples DAG and CaScience advances · 2026Article
- Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Biomimetic Analysis of Neurotransmitters for Disease Diagnosis through Light-Driven Nanozyme Sensor Array and Machine Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Estimates of quantal synaptic parameters in light of more complex vesicle pool models.Frontiers in cellular neuroscience · 2025Article
- Different states of synaptic vesicle priming explain target cell type-dependent differences in neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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3 authors at 3 institutions in 1 country.
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Abstract
Pronounced differences in neurotransmitter release from a given presynaptic neuron, depending on the synaptic target, are among the most intriguing features of cortical networks. Hippocampal pyramidal cells (PCs) release glutamate with low probability to somatostatin expressing oriens-lacunosum-moleculare (O-LM) interneurons (INs), and the postsynaptic responses show robust short-term facilitation, whereas the release from the same presynaptic axons onto fast-spiking INs (FSINs) is ~10-fold higher and the excitatory postsynaptic currents (EPSCs) display depression. The mechanisms underlying these vastly different synaptic behaviors have not been conclusively identified. Here, we applied a combined functional, pharmacological, and modeling approach to address whether the main difference lies in the action potential-evoked fusion or else in upstream priming processes of synaptic vesicles (SVs). A sequential two-step SV priming model was fitted to the peak amplitudes of unitary EPSCs recorded in response to complex trains of presynaptic stimuli in acute hippocampal slices of adult mice. At PC-FSIN connections, the fusion probability (P
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