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

Glial activation and pathological pain.

Julie Wieseler-Frank1, Steven F Maier, Linda R Watkins

  • 1Department of Psychology, Center for Neuroscience, University of Colorado at Boulder, Boulder, CO 80309-0345, USA. frankjw@psych.colorado.edu

Neurochemistry International
|May 18, 2004
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

Pain and the immune system.

Musculoskeletal science & practice·2026
Same author

Caudal Granular Insular Cortex to Somatosensory Cortex I: A Critical Pathway for the Transition of Acute to Chronic Pain.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2025
Same author

Reordering neuroimmune signaling to prevent and resolve chronic pain.

Pain·2025
Same author

Activation of sphingosine-1-phosphate receptor subtype 1 in the central nervous system contributes to morphine-induced hyperalgesia and antinociceptive tolerance in rodents: erratum.

Pain·2025
Same author

An initial investigation of transcutaneous delivery of plasmid DNA encoding interleukin-10 for the treatment of psoriatic skin conditions.

Brain, behavior, and immunity·2024
Same author

Prevention and reversal of neuropathic pain by near-infrared photobiomodulation therapy in male and female rats.

Physiology & behavior·2024

Pathological pain involves overactive glial cells (astrocytes and microglia) releasing inflammatory cytokines. These glia, not just neurons, are key targets for new pain therapies.

Area of Science:

  • Neuroscience
  • Immunology
  • Pain Research

Background:

  • Pathological pain involves persistent, amplified pain responses.
  • Traditionally attributed to neuronal dysfunction, glial cell involvement is increasingly recognized.

Purpose of the Study:

  • To review the role of glia, specifically astrocytes and microglia, in pathological pain.
  • To highlight glia as potential therapeutic targets for pain management.

Main Methods:

  • Review of existing scientific literature on glia and pain.
  • Analysis of signaling pathways involving substance P, glutamate, and fractalkine in glial activation.
  • Examination of the role of proinflammatory cytokines and gap junctions.

Main Results:

Related Experiment Videos

  • Astrocytes and microglia are activated by neuronal signals in pathological pain.
  • Activated glia release mediators, including proinflammatory cytokines, that sustain exaggerated pain.
  • Astrocyte gap junction communication may mediate pain spread (extra-territorial, mirror-image pain).

Conclusions:

  • Glia are critical mediators of pathological pain, extending beyond neuronal targets.
  • Targeting glial-neuronal interactions offers novel therapeutic strategies for pain.
  • These interactions may also influence other behavioral phenomena.