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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
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Updated: Apr 10, 2026

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
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Selective, genetically induced increase in synaptic vesicle priming.

Mohammad Aldahabi1, Flora Balint1, Andrea Lorincz1

  • 1Laboratory of Cellular Neurophysiology, HUN-REN Institute of Experimental Medicine, Budapest 1083, Hungary.

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|April 8, 2026
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Summary
This summary is machine-generated.

Synaptic vesicle (SV) priming, not fusion, dictates neurotransmitter release probability. Enhancing SV priming increases synaptic strength by boosting the number of readily releasable vesicles, offering new insights into synaptic function.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Synaptic vesicle (SV) release probability (Pv) depends on vesicle priming and fusion probability (Pfusion).
  • Disentangling the roles of SV priming and fusion in synaptic function is challenging.
  • SV priming is increasingly recognized as crucial for synaptic diversity.

Purpose of the Study:

  • To develop a method for selectively and inducibly enhancing SV priming.
  • To investigate the impact of increased SV priming on synaptic transmission.
  • To determine the relative contributions of SV priming and fusion to synaptic variability.

Main Methods:

  • Generated a mouse model with a Munc13-1 mutation (H567K) to enhance its function.
  • Utilized Cre-dependent allele removal for cell type-specific Munc13-1 enhancement.
  • Measured excitatory postsynaptic current (EPSC) amplitude and quantal size at hippocampal synapses.

Main Results:

  • Selective enhancement of Munc13-1 function increased SV release probability (Pv).
  • Increased Pv resulted from a higher proportion of primed SVs, not altered fusion probability (Pfusion).
  • Synaptic strength variability is primarily driven by differences in SV priming.

Conclusions:

  • SV priming is the dominant factor determining presynaptic release probability.
  • Enhanced SV priming leads to increased synaptic efficacy without altering quantal size.
  • Variability in postsynaptic target cell type influences presynaptic release through modulation of SV priming.