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 Experiment Videos

Synaptic vesicles: half full or half empty?

Thomas S Hnasko1, Robert H Edwards

  • 1Department of Neurology, School of Medicine, University of California-San Francisco, 600 16th Street, GH-N272B, San Francisco, CA 94158, USA.

Neuron
|September 5, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

When Inhibition Fails: Adolescent Nicotine Disrupts Opioid Control of Ventral Tegmental Area GABA Neurons.

Biological psychiatry·2026
Same author

GABA-glutamate corelease is a mechanism for state-dependent neurotransmission.

bioRxiv : the preprint server for biology·2025
Same author

Synaptic vesicles that store monoamines and glutamate differ in protein composition.

bioRxiv : the preprint server for biology·2025
Same author

Mu-opioid receptor activation potentiates excitatory transmission at the habenulo-peduncular synapse.

Cell reports·2025
Same author

Parkinson's Disease-vulnerable and -resilient dopamine neurons display opposite responses to excitatory input.

bioRxiv : the preprint server for biology·2025
Same author

Substrate recognition and allosteric regulation of synaptic vesicle glutamate transporter VGLUT2.

Nature structural & molecular biology·2025
Same journal

Fast-conducting mechanonociceptors uniquely engage reflexive and affective pain circuitry to drive protective responses.

Neuron·2026
Same journal

Sparse component analysis: A method that uncovers separable computations within neural population activity.

Neuron·2026
Same journal

Spatiomolecular mapping reveals anatomical organization of heterogeneous cell types in the human nucleus accumbens.

Neuron·2026
Same journal

TGF-β1-induced endothelial transcytosis drives blood-brain barrier leakage during aging.

Neuron·2026
Same journal

Image space opens up for visual neuroscience.

Neuron·2026
Same journal

Septal GLP-1 receptors control alcohol taking and seeking.

Neuron·2026
See all related articles

Changes in transporter expression altering quantal size can impact behavior. This study highlights presynaptic mechanisms, specifically vesicular transporters, as key regulators of synaptic plasticity and neuronal function.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Investigates presynaptic mechanisms regulating quantal size, a key aspect of synaptic plasticity.
  • Focuses on vesicular transporters' role in filling synaptic vesicles with neurotransmitters.
  • Explores how presynaptic regulation, rather than postsynaptic, influences synaptic strength.

Discussion:

  • Prado et al. demonstrate that alterations in transporter expression directly affect quantal size.
  • This modulation of quantal size by presynaptic mechanisms has significant implications for neural circuit function.
  • Highlights the adaptability of synaptic transmission through presynaptic control.

Key Insights:

  • Changes in vesicular transporter expression can modify quantal size.

Related Experiment Videos

  • Quantal size alterations mediated by presynaptic mechanisms influence observable behavior.
  • Vesicular transporters are critical targets for regulating synaptic efficacy.
  • Outlook:

    • Further research into transporter regulation could reveal novel therapeutic targets for neurological disorders.
    • Understanding these presynaptic mechanisms is crucial for deciphering complex neural computations.
    • This work opens new avenues for exploring activity-dependent synaptic modifications.