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

Norepinephrine release from spinal synaptosomes: auto-alpha2 -adrenergic receptor modulation.

X Li1, Z Zhao, H L Pan

  • 1Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1009, USA.

Anesthesiology
|June 22, 2000
PubMed
Summary

Clonidine inhibits norepinephrine release in the spinal cord via alpha2-adrenergic receptors, likely the alpha2A subtype. This suggests indirect actions mediate clonidine

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

Advances in Head and Neck Cancer Pain.

Journal of dental research·2022
Same author

Heat Stability of the Bile Salt-Stimulated Lipase in Human Milk Fortified with Sodium Taurocholate <sup>1</sup>.

Journal of food protection·2019
Same author

Capsaicin-induced pain and sensitisation in the postpartum period.

British journal of anaesthesia·2018
Same author

Fraud in anesthesia - an editor's perspective.

Revista espanola de anestesiologia y reanimacion·2014
Same author

The puerperium alters spinal cord plasticity following peripheral nerve injury.

Neuroscience·2012
Same author

Opioid-independent mechanisms supporting offset analgesia and temporal sharpening of nociceptive information.

Pain·2012

Area of Science:

  • Neuroscience
  • Pharmacology
  • Adrenergic receptor research

Background:

  • Clonidine (CLON) provides spinal analgesia by activating alpha2-adrenergic receptors.
  • Recent studies show CLON increases spinal norepinephrine (NE) release in vivo, contrary to expected presynaptic autoinhibition.
  • This study investigates CLON's effect on NE release in spinal cord tissue without synaptic circuits.

Purpose of the Study:

  • To determine if clonidine inhibits norepinephrine release in spinal cord tissue lacking synaptic circuits.
  • To investigate the role of alpha2-adrenergic receptors in clonidine's effect on NE release.
  • To explore the subtype specificity of alpha2-adrenergic receptors involved.

Main Methods:

  • Preparation of crude synaptosomes from rat spinal cord.

Related Experiment Videos

  • Loading synaptosomes with [3H]NE and stimulating NE release with potassium chloride.
  • Incubation with clonidine and various inhibitors, including alpha2-adrenergic antagonists.
  • Utilizing antisense oligodeoxynucleotides (ODN) to investigate alpha2A-adrenergic receptor subtypes.

    • Main Results:

    • Potassium chloride-induced [3H]NE release was inhibited by clonidine (IC50 = 1.3 microm).
    • Clonidine's inhibitory effect was blocked by alpha2-adrenergic antagonists (yohimbine, idazoxan) but not alpha1, muscarinic, or opioid antagonists.
    • Antisense ODN targeting alpha2A-adrenergic receptors reduced receptor expression and clonidine-induced inhibition of NE release.

    Conclusions:

    • Classic autoinhibitory alpha2-adrenergic receptors, likely alpha2A subtype, exist in the spinal cord.
    • Clonidine-induced stimulation of spinal NE release likely results from indirect actions via spinal circuits.