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

Nitric oxide modulates synaptic vesicle docking fusion reactions

M K Meffert1, N C Calakos, R H Scheller

  • 1Department of Neurobiology, Stanford University School of Medicine, California 94305, USA.

Neuron
|June 1, 1996
PubMed
Summary

Nitric oxide (NO) enhances neurotransmitter release by altering synaptic protein interactions. This process involves modifying sulfhydryl groups, impacting vesicle docking and fusion for synaptic plasticity.

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

Sedimentation rate and suPAR in relation to disease activity and mortality in patients with tuberculosis.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2019
Same author

CT and US features of cervical lymphadenopathy due to kikuchi's disease.

Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India·2012
Same author

A proteomic study of serum from children with autism showing differential expression of apolipoproteins and complement proteins.

Molecular psychiatry·2006
Same author

Roles for NF-kappaB in nerve cell survival, plasticity, and disease.

Cell death and differentiation·2006
Same author

The molecular basis of CaMKII function in synaptic and behavioural memory.

Nature reviews. Neuroscience·2002
Same author

Upper airway obstruction-related sleep apnea in a child with thalassemia intermedia.

Journal of pediatric hematology/oncology·2002

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) is a signaling molecule involved in various physiological processes.
  • Neurotransmitter release from synaptosomes is crucial for synaptic transmission.
  • Synaptic vesicle docking and fusion are regulated by a complex of proteins.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in calcium-independent neurotransmitter release.
  • To elucidate the molecular mechanisms by which NO influences synaptic vesicle fusion.
  • To identify the specific synaptic proteins modulated by NO.

Main Methods:

  • Experiments using synaptosomes and recombinant proteins.
  • Application of NO donors and inhibitors like Botulinum neurotoxins, NEM, and beta-ME.

Related Experiment Videos

  • Analysis of protein-protein interactions within the synaptic core complex.

    • Main Results:

    • NO stimulates calcium-independent neurotransmitter release.
    • Botulinum neurotoxins inhibit NO-stimulated release.
    • NO donors promote the formation of the VAMP/SNAP-25/syntaxin 1a core complex.
    • NO inhibits the binding of n-sec1 to syntaxin 1a.
    • Post-translational modification of sulfhydryl groups by NO appears to regulate these interactions.

    Conclusions:

    • Nitric oxide (NO) modulates synaptic protein interactions to regulate neurotransmitter release.
    • NO likely acts via post-translational modification of sulfhydryl groups on synaptic proteins.
    • These findings suggest a novel mechanism for NO in synaptic plasticity.