Related Experiment Video
Updated: Aug 7, 2026
13:02
Sagittal Plane Kinematic Gait Analysis in C57BL/6 Mice Subjected to MOG35-55 Induced Experimental Autoimmune Encephalomyelitis
Published on: November 4, 2017
Spinal motoneurone distress during experimental allergic encephalomyelitis
L Giardino1, A Giuliani, M Fernandez
1Department of Veterinary Morphophysiology and Animal Production (DIMORFIPA), University of Bologna, Ozzano dell'Emilia, Italy.
Neuropathology and Applied Neurobiology
|October 19, 2004
Summary
In experimental allergic encephalomyelitis (EAE), a multiple sclerosis model, spinal cord gliosis impacts motoneurone function. This study reveals how glial activation affects key neurotransmitter synthesis during the disease process.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Multiple sclerosis (MS) is primarily characterized by demyelination.
- Neural damage is increasingly recognized as a factor in chronic MS.
- Experimental allergic encephalomyelitis (EAE) serves as a key animal model for MS research.
Purpose of the Study:
- To investigate microglial activation and astrocytosis in the spinal cord during EAE.
- To examine the regulation of choline acetyl-transferase (ChAT) and calcitonin gene-related peptide (CGRP) mRNA in spinal motoneurones during EAE.
- To understand the impact of gliosis on neuronal function in an MS model.
Main Methods:
- EAE induced in female Lewis rats using guinea pig spinal cord tissue and complete Freund's adjuvant (CFA).
- Control groups included rats injected with CFA and uninjected rats.
- In situ hybridization used to quantify ChAT and CGRP mRNA levels in the lumbar spinal cord.
- Computerized grain counting for mRNA quantification.
Main Results:
- ChAT mRNA levels were significantly reduced at 14 days post-immunization in EAE rats, with subsequent recovery.
- CGRP mRNA levels increased at 14 days post-immunization, then returned to control levels.
- Extensive and persistent gliosis observed in the spinal cord, surrounding motoneurones.
- Transient expression of p75LNGFR noted in motoneurones.
Conclusions:
- EAE involves significant microglial activation and astrocytosis in the spinal cord.
- Gliosis in EAE models induces neuronal distress, affecting neurotransmitter synthesis enzymes.
- These findings highlight the role of glial responses in neuronal dysfunction during MS pathogenesis.
