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

You might also read

Related Articles

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

Sort by
Same author

Inflammatory Mediators Both Directly and Indirectly Promote Microglial Proliferation.

Glia·2026
Same author

Plagl1 regulates the retinal progenitor cell to Müller glial cell transition.

PLoS genetics·2026
Same author

Peripheral immune response and axonal degeneration in the hind paw skin of mice with experimental autoimmune encephalomyelitis.

Neurobiology of pain (Cambridge, Mass.)·2026
Same author

Age-impaired remyelination is associated with dysregulated microglial transitions.

Nature communications·2025
Same author

Sex-specific involvement of calcitonin gene-related peptide signaling for pain in experimental autoimmune encephalomyelitis.

Pain reports·2025
Same author

CSF1R ligands promote microglial proliferation but are not the sole regulators of developmental microglial proliferation.

Development (Cambridge, England)·2025

Related Experiment Video

Updated: May 15, 2026

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
08:17

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis

Published on: February 23, 2024

Changes in nociceptive sensitivity and object recognition in experimental autoimmune encephalomyelitis (EAE).

Camille J Olechowski1, Gustavo Tenorio, Yves Sauve

  • 1Centre for Neuroscience, University of Alberta, Edmonton, AB, Canada.

Experimental Neurology
|January 8, 2013
PubMed
Summary
This summary is machine-generated.

Multiple sclerosis (MS) causes pain and cognitive issues. Treating spinal glutamate transporter changes with ceftriaxone improved pain and object recognition in an MS animal model.

More Related Videos

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
06:19

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Published on: September 9, 2022

Related Experiment Videos

Last Updated: May 15, 2026

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
08:17

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis

Published on: February 23, 2024

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
06:19

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Published on: September 9, 2022

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Multiple sclerosis (MS) is linked to depression, cognitive deficits, and neuropathic pain.
  • Tactile allodynia (hypersensitivity to touch) is present at disease onset in the experimental autoimmune encephalomyelitis (EAE) model of MS.

Purpose of the Study:

  • To investigate cognitive impairments in EAE mice.
  • To determine if altered nociceptive sensitivity correlates with cognitive deficits in EAE.
  • To explore the role of spinal IL-1β, IL-6, and EAAT-2 in EAE-associated pain and cognitive dysfunction.

Main Methods:

  • Monitoring object recognition in EAE mice using the novel object recognition (NOR) assay.
  • Analyzing spinal gene expression of IL-1β, IL-6, and EAAT-2.
  • Assessing EAAT-2 protein levels in the spinal cord.
  • Treating EAE mice with ceftriaxone to modulate glutamate transporter levels.

Main Results:

  • EAE mice exhibited impaired performance in the NOR assay, indicating cognitive deficits early in the disease.
  • Increased spinal expression of IL-1β, IL-6, and EAAT-2 mRNA was observed, coinciding with hypersensitivity and cognitive deficits.
  • A decrease in spinal EAAT-2 protein levels was detected in EAE mice.
  • Ceftriaxone treatment reversed tactile hypersensitivity and normalized NOR assay performance in EAE mice.

Conclusions:

  • Spinal changes in glutamate transporter EAAT-2 are linked to both pain hypersensitivity and cognitive impairment in experimental autoimmune encephalomyelitis.
  • Targeting spinal pain mechanisms, specifically glutamate transporter dysregulation, offers a potential therapeutic strategy for cognitive deficits in MS.
  • There is a significant interplay between pain and cognitive function in MS, suggesting shared underlying mechanisms.