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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.
Abstract:
The main pathophysiological feature characterizing multiple sclerosis (MS) is demyelination. However, the possibility of neural damage has recently been proposed as a mechanism in chronic disease. Experimental allergic encephalomyelitis (EAE) is the most widely used experimental model for MS. We investigated occurrences of microglial activation and astrocytosis in the spinal cord, choline acetyl-transferase (ChAT) and calcitonin gene-related peptide (CGRP) mRNA regulation in spinal motoneurones during EAE. EAE was induced in female Lewis rats by injecting guinea pig spinal cord tissue in complete Freund's adjuvant (CFA) to which heat-inactivated Mycobacterium had been added. Rats injected with CFA and uninjected rats were used as controls. ChAT and CGRP mRNAs were studied by in situ hybridization in the lumbar spinal cord and a computerized grain counting procedure was used for quantification. No differences in ChAT mRNA level were found between control and CFA-injected rats. ChAT mRNA level was strongly reduced in EAE 14 days after immunization and then recovered (29 days after immunization). CGRP mRNA increased 14 days after immunization, and then recovered to control level. Extensive long-lasting gliosis developed in the spinal cord and around motoneurones and a transient expression of p75LNGFR in motoneurones was also found. These data suggest that during EAE, gliosis induces distress in spinal cord neurones involving the synthesis enzyme for the main transmitter.
Insights
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.
