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

Synaptic Signaling01:09

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Synaptic Signaling01:12

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

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...
Chemical Synapses01:26

Chemical Synapses

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...
Chemical Synapses01:26

Chemical Synapses

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...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

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 to...

You might also read

Related Articles

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

Sort by
Same author

Costunolide and dehydrocostus lactone alleviate ulcerative colitis via regulating TLR4, NF-κB and PI3K expression.

Scientific reports·2024
Same author

Virtual Screening and Biological Evaluation of Natural Products as Novel VPS34 Inhibitors that Modulate Autophagy.

ChemMedChem·2024
Same author

Overabundant endocannabinoids in neurons are detrimental to cognitive function.

bioRxiv : the preprint server for biology·2024
Same author

QBT improved cognitive dysfunction in rats with vascular dementia by regulating the Nrf2/xCT/GPX4 and NLRP3/Caspase-1/GSDMD pathways to inhibit ferroptosis and pyroptosis of neurons.

International immunopharmacology·2024
Same author

High salt condition alters LPS synthesis and induces the emergence of drug resistance mutations in <i>Helicobacter pylori</i>.

Antimicrobial agents and chemotherapy·2024
Same author

Free medial femoral condyle osteocutaneous flap for repairing stage IIIB osteonecrosis of the lunate: a case report.

BMC musculoskeletal disorders·2024

Related Experiment Video

Updated: Jul 4, 2026

FM Dye Cycling at the Synapse: Comparing High Potassium Depolarization, Electrical and Channelrhodopsin Stimulation
08:31

FM Dye Cycling at the Synapse: Comparing High Potassium Depolarization, Electrical and Channelrhodopsin Stimulation

Published on: May 24, 2018

Cyclooxygenase-2 in synaptic signaling.

Hongwei Yang1, Chu Chen

  • 1Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA. cchen@lsuhsc.edu

Current Pharmaceutical Design
|June 10, 2008
PubMed
Summary
This summary is machine-generated.

Cyclooxygenase-2 (COX-2) plays a dual role in brain function by metabolizing both arachidonic acid and endocannabinoids. Understanding these pathways is key to developing treatments for neuroinflammation and neurological disorders.

More Related 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

Channelrhodopsin2 Mediated Stimulation of Synaptic Potentials at Drosophila Neuromuscular Junctions
09:12

Channelrhodopsin2 Mediated Stimulation of Synaptic Potentials at Drosophila Neuromuscular Junctions

Published on: March 16, 2009

Related Experiment Videos

Last Updated: Jul 4, 2026

FM Dye Cycling at the Synapse: Comparing High Potassium Depolarization, Electrical and Channelrhodopsin Stimulation
08:31

FM Dye Cycling at the Synapse: Comparing High Potassium Depolarization, Electrical and Channelrhodopsin Stimulation

Published on: May 24, 2018

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

Channelrhodopsin2 Mediated Stimulation of Synaptic Potentials at Drosophila Neuromuscular Junctions
09:12

Channelrhodopsin2 Mediated Stimulation of Synaptic Potentials at Drosophila Neuromuscular Junctions

Published on: March 16, 2009

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Cyclooxygenase-2 (COX-2) is crucial in neuroinflammation and implicated in neurodegenerative diseases.
  • COX-2 activity affects synaptic function, neurotransmission, and long-term potentiation (LTP).
  • Its role extends beyond prostaglandin synthesis to include endocannabinoid metabolism.

Purpose of the Study:

  • To investigate the dual role of COX-2 in synaptic signaling.
  • To explore COX-2's metabolism of endocannabinoids and its downstream effects.
  • To provide a mechanistic basis for novel therapeutic strategies.

Main Methods:

  • Review of existing literature on COX-2, prostaglandins, and endocannabinoids.
  • Analysis of signaling pathways involved in COX-2 mediated neuroinflammation.
  • Examination of COX-2's role in synaptic plasticity and neurodegeneration.

Main Results:

  • COX-2 metabolizes arachidonic acid to prostaglandins (e.g., PGE(2)) influencing neurotransmission via the EP(2)/PKA pathway.
  • COX-2 also oxygenates endocannabinoids into novel prostaglandins.
  • These novel metabolites modulate synaptic transmission and plasticity through MAPK and IP(3) pathways, contributing to neurodegeneration.

Conclusions:

  • COX-2's contribution to neurological disorders involves both classic prostaglandin synthesis and endocannabinoid metabolism.
  • Novel COX-2 metabolites of endocannabinoids are significant signaling mediators.
  • Targeting COX-2 pathways offers potential for treating neuroinflammation-associated neurological disorders.