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

Presynaptic modulation by eicosanoids in cortical synaptosomes

G Zoltay1, J R Cooper

  • 1Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510.

Neurochemical Research
|September 1, 1994
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

Questioning the Cuprate Paradigm: Absence of Superfluid Density Loss in Several Overdoped Cuprates I.

Physical review letters·2026
Same author

Charge density waves and Fermi surface reconstruction in the clean overdoped cuprate superconductor Tl<sub>2</sub>Ba<sub>2</sub>CuO<sub>6+δ</sub>.

Nature communications·2022
Same author

Incoherent transport across the strange-metal regime of overdoped cuprates.

Nature·2021
Same author

Thermoelectric quantum oscillations in ZrSiS.

Nature communications·2017
Same author

Metrological challenges for measurements of key climatological observables: Oceanic salinity and pH, and atmospheric humidity. Part 1: Overview.

Metrologia·2016
Same author

Metrological challenges for measurements of key climatological observables, Part 4: Atmospheric relative humidity.

Metrologia·2016
Same journal

Correction to: Dual Antioxidant DH-217 Mitigated Cerebral Ischemia-Reperfusion Injury by Targeting IKKβ/Nrf2/HO-1 Signal Axis.

Neurochemical research·2026
Same journal

Microglia-Dependent BDNF Signaling in the Dentate Gyrus Underlies the Antidepressant Effects of Gardiquimod, a Toll-Like Receptor 7 Agonist, in Chronically Stressed Mice.

Neurochemical research·2026
Same journal

Cryptotanshinone Targets Ferroptosis in Glioma via the EGFR/ROS Signaling Pathway.

Neurochemical research·2026
Same journal

Combined Puerarin and Magnesium Acetyl Taurate Intervention Mitigates Autism-Like Pathology Through Glutamatergic and MAPK Pathway Regulation.

Neurochemical research·2026
Same journal

Long-Term Impact of Early-Life Stress on Hippocampal Apoptotic Gene Expression in BALB/c Mice.

Neurochemical research·2026
Same journal

Minute-Resolution Sampling Reveals Rapid and Stimulus-Specific IL-1β Dynamics During Acute Epileptiform Activity.

Neurochemical research·2026
See all related articles

Inhibitory presynaptic modulators activate potassium (K+) channels via eicosanoids, decreasing neurotransmitter release. This research uncovers a novel signaling pathway in the brain.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Cellular Signaling

Background:

  • Inhibitory presynaptic modulation is crucial for regulating neuronal activity.
  • The precise ionic mechanisms underlying presynaptic inhibition require further elucidation.

Purpose of the Study:

  • To investigate the ionic basis of inhibitory presynaptic modulation.
  • To identify the second messengers involved in this process.

Main Methods:

  • Utilized rat cortical synaptosomes and a K+-sensitive electrode to measure potassium efflux.
  • Examined the effects of various receptor agonists and inhibitors on K+ efflux.

Main Results:

  • Activation of purinergic, adrenergic, muscarinic, and opioid receptors promoted K+ efflux.

Related Experiment Videos

  • 2-chloroadenosine-induced K+ efflux was blocked by indomethacin, implicating arachidonic acid metabolites.
  • Arachidonic acid and PGE2 increased K+ efflux, inhibited by dendrotoxin and mast cell degranulating peptide.

    • Conclusions:

    • Inhibitory presynaptic modulators utilize eicosanoid second messengers to open a specific class of K+ channels.
    • These channels hyperpolarize nerve terminals, reducing Ca2+ influx and subsequent neurotransmitter release.