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

Spinal mechanisms contributing to joint pain.

Hans-Georg Schaible1

  • 1Department of Physiology, Friedrich-Schiller-University of Jena, Teichgraben 8, D-07740 Jena, Germany.

Novartis Foundation Symposium
|July 31, 2004
PubMed
Summary

Joint inflammation causes spinal cord neurons to become hyperexcitable, altering pain processing. This neuroplastic change, involving specific neurotransmitters, persists with chronic inflammation.

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

[The journal "Der Schmerz"-40th anniversary].

Schmerz (Berlin, Germany)·2026
Same author

Sympathosensory interactions - Possible relevance in osteoarthritis.

Osteoarthritis and cartilage·2025
Same author

[Chronic pain and comorbidity : Just an added burden-or also an opportunity?]

Schmerz (Berlin, Germany)·2025
Same author

[What does pain have to do with neuronal networks and the afferent matrix?]

Orthopadie (Heidelberg, Germany)·2025
Same author

[The importance of health care research for the medical community from the perspective of the German Pain Society].

Schmerz (Berlin, Germany)·2025
Same author

Do cytokines play a role in the transition from acute to chronic musculoskeletal pain?

Pharmacological research·2025

Area of Science:

  • Neuroscience
  • Pain Research
  • Spinal Cord Physiology

Background:

  • Nociceptive signals from joints are processed by various spinal cord neurons.
  • These neurons exhibit different response patterns to mechanical stimuli from skin, muscles, and joints.
  • Joint inflammation induces significant changes in spinal nociceptive processing.

Purpose of the Study:

  • To investigate the neuroplastic changes in spinal cord neurons during joint inflammation.
  • To understand the alterations in nociceptive processing due to inflammation.
  • To identify the role of descending inhibition and neurochemical mediators in inflammation-induced hyperexcitability.

Main Methods:

  • Analysis of spinal cord neuron responses to mechanical stimulation in inflamed joints.
  • Assessment of neuronal hyperexcitability, receptive field size, and mechanical thresholds.
  • Investigation of the influence of descending inhibition.
  • Examination of neurotransmitter and mediator release patterns during inflammation.

Main Results:

  • Joint inflammation leads to pronounced hyperexcitability in spinal neurons receiving joint input.
  • This includes enhanced responses, reduced mechanical thresholds, and expanded receptive fields.
  • Inflammation-induced hyperexcitability is maintained during persistent inflammation.
  • Descending inhibition increases during the acute phase of inflammation.
  • Neurotransmitters like glutamate, substance P, CGRP, and prostaglandins are implicated.

Conclusions:

  • Inflammation induces neuroplastic changes in the spinal cord, altering nociceptive processing.
  • These changes result in a state of neuronal hyperexcitability that persists.
  • Descending inhibition and various chemical mediators play crucial roles in this process.

Related Experiment Videos