Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Fusion of Secretory Vesicles with the Plasma Membrane01:26

Fusion of Secretory Vesicles with the Plasma Membrane

19.6K
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.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
19.6K
Long-term Potentiation01:35

Long-term Potentiation

59.6K
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.
59.6K
Long-term Potentiation01:25

Long-term Potentiation

3.9K
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.
Hebbian LTP
LTP can occur when...
3.9K
Overview of Secretory Vesicles01:33

Overview of Secretory Vesicles

10.1K
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.
Various proteins regulate the aggregation of molecules inside the secretory vesicles. Chromogranins...
10.1K
Integration of Synaptic Events01:28

Integration of Synaptic Events

6.1K
Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
6.1K
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

1.2K
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
1.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction.

Science translational medicine·2026
Same author

Encephalopathy-linked UFM1 variants impede neuronal protein translation, development, and function.

EMBO molecular medicine·2026
Same author

Munc13-1 couples DAG and Ca<sup>2+</sup> signaling to dynamic vesicle priming, synaptic short-term plasticity, and posttetanic potentiation.

Science advances·2026
Same author

CDC42-Effector Proteins Regulate Higher Order Structure of Septins Required for CNS Myelin Integrity.

Glia·2026
Same author

A general one-step protocol to generate impermeable fluorescent HaloTag substrates for in situ live cell application and super-resolution imaging.

Nature communications·2026
Same author

GARLH regulates neuroligin preference for excitatory versus inhibitory synapses.

The Journal of cell biology·2025
Same journal

Erratum for the Research Article "Assessing the health risks of rice cadmium content standards in China" by H. Chu <i>et al</i>.

Science advances·2026
Same journal

Erratum for the Research Article "Developmental regulation of Erk signaling by mitotic kinases" by F. Chen <i>et al</i>.

Science advances·2026
Same journal

Magnetically levitated metasurface enabling tangible and bidirectional human-machine interaction.

Science advances·2026
Same journal

A general photoinduced manganese-catalyzed platform for the sequential difunctionalization of [1.1.1]propellane.

Science advances·2026
Same journal

Turning sound and force into light with AlN:Mn<sup>2+</sup> mechanoluminescence.

Science advances·2026
Same journal

Extreme dominance of Earth-origin heavy ions in the intense ring current near the Earth during the May 2024 super geomagnetic storm.

Science advances·2026
See all related articles
  1. Home
  3. Selective, Genetically Induced Increase In Synaptic Vesicle Priming.
  1. Home
  3. Selective, Genetically Induced Increase In Synaptic Vesicle Priming.

Related Experiment Video

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

8.1K

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.

Science Advances
|April 8, 2026

View abstract on PubMed

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.

More Related Videos

Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
08:06

Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient

Published on: September 3, 2014

32.2K
Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes
09:02

Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes

Published on: November 11, 2011

15.7K

Related Experiment Videos

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

8.1K
Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
08:06

Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient

Published on: September 3, 2014

32.2K
Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes
09:02

Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes

Published on: November 11, 2011

15.7K

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.