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

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

6.8K
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
6.8K
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

3.9K
Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
3.9K
Chemical Synapses01:26

Chemical Synapses

8.5K
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
8.5K
Chemical Synapses01:26

Chemical Synapses

12.4K
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
12.4K
Protein Modifications in the RER01:26

Protein Modifications in the RER

7.6K
Modification of secretory and transmembrane proteins entering the rough ER begins in the ER lumen. These modifications aid in protein folding and stabilize the acquired tertiary structure. Protein modifications in the rough ER co-occur at different stages of protein folding.
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal...
7.6K
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

14.7K
When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
14.7K

You might also read

Related Articles

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

Sort by
Same author

Physiological oxygen levels reset K<sup>+</sup> channel activity in human vascular endothelial cells.

Redox biology·2026
Same author

High fat diet induces differential age- and gender-dependent changes in neuronal function in Drosophila linked to redox stress.

Behavioural brain research·2025
Same author

Neuroinflammation in Alzheimer disease.

Nature reviews. Immunology·2024
Same author

Plum modulates Myoglianin and regulates synaptic function in <i>D. melanogaster</i>.

Open biology·2023
Same author

Medium-Chain Fatty Acids Rescue Motor Function and Neuromuscular Junction Degeneration in a <i>Drosophila</i> Model of Amyotrophic Lateral Sclerosis.

Cells·2023
Same author

Redox mechanisms and their pathological role in prion diseases: The road to ruin.

PLoS pathogens·2023

Related Experiment Video

Updated: Mar 29, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO&#8226;) Probes, the geNOps, for Real-time Imaging of NO&#8226; Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

13.4K

Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse.

Sophie A Bradley1, Joern R Steinert1

  • 1MRC Toxicology Unit, Hodgkin Building, Leicester LE1 9HN, UK.

Oxidative Medicine and Cellular Longevity
|December 5, 2015
PubMed
Summary

Nitric oxide (NO) is vital for brain function, impacting synaptic plasticity and neuronal survival. Dysregulation of NO signaling, through S-nitrosylation, contributes to neurodegenerative diseases like Alzheimer's and Parkinson's.

More Related Videos

Preparation of Synaptoneurosomes from Mouse Cortex using a Discontinuous Percoll-Sucrose Density Gradient
08:30

Preparation of Synaptoneurosomes from Mouse Cortex using a Discontinuous Percoll-Sucrose Density Gradient

Published on: September 17, 2011

33.1K
Presynaptically Silent Synapses Studied with Light Microscopy
11:02

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

11.9K

Related Experiment Videos

Last Updated: Mar 29, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO&#8226;) Probes, the geNOps, for Real-time Imaging of NO&#8226; Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

13.4K
Preparation of Synaptoneurosomes from Mouse Cortex using a Discontinuous Percoll-Sucrose Density Gradient
08:30

Preparation of Synaptoneurosomes from Mouse Cortex using a Discontinuous Percoll-Sucrose Density Gradient

Published on: September 17, 2011

33.1K
Presynaptically Silent Synapses Studied with Light Microscopy
11:02

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

11.9K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) is a key gasotransmitter in the nervous system, regulating physiological processes.
  • NO influences synaptic plasticity (LTP/LTD) and neuronal survival through various signaling pathways.
  • Emerging research highlights NO's role in post-translational modifications beyond canonical cGMP signaling.

Purpose of the Study:

  • To review the multifaceted roles of NO in synaptic transmission and vesicular release.
  • To explore the impact of S-nitrosylation and 3-nitrotyrosination on protein function.
  • To differentiate NO's physiological functions from its pathological roles in neurodegeneration.

Main Methods:

  • Literature review focusing on nitrergic signaling.
  • Analysis of protein post-translational modifications (S-nitrosylation, 3-nitrotyrosination).
  • Examination of NO's involvement in synaptic transmission and vesicular release.

Main Results:

  • NO modulates synaptic transmission and vesicular release via pre- and postsynaptic mechanisms.
  • S-nitrosylation and 3-nitrotyrosination are critical post-translational modifications affecting protein function.
  • NO signaling is crucial for normal brain function, including synaptic plasticity and neuronal survival.

Conclusions:

  • NO plays a dual role in the brain, essential for normal function but implicated in disease when dysregulated.
  • Aberrant NO signaling and excessive nitrosative stress contribute to neurodegenerative diseases.
  • Understanding NO's complex roles is vital for developing therapeutic strategies for neurological disorders.