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Nociception

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the...

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Mechanical hypernociception in experimental autoimmune encephalomyelitis.

David Henrique Rodrigues¹, Daniela Sachs, Antonio Lucio Teixeira

¹Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.

Arquivos De Neuro-Psiquiatria

|March 31, 2009

Summary

This study shows that mice with experimental autoimmune encephalomyelitis (EAE) experience increased pain sensitivity before motor symptoms appear. This validates the MOG35-55 EAE model for studying pain in multiple sclerosis.

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Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice

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Published on: November 9, 2017

Area of Science:

Neuroscience
Immunology
Pain Research

Background:

Pain is a significant but understudied clinical symptom in multiple sclerosis (MS).
Understanding pain mechanisms in MS is crucial for improving patient care.

Purpose of the Study:

To investigate nociceptive responses in mice with MOG35-55 induced experimental autoimmune encephalomyelitis (EAE).
To establish the MOG35-55 EAE model as a viable tool for pain research in MS.

Main Methods:

Experimental autoimmune encephalomyelitis (EAE) was induced in female C57BL/6 mice using MOG35-55 emulsion and adjuvants.
Nociception was assessed using the von Frey filaments method.
Motor impairment was evaluated using a clinical scale (0-15).

Main Results:

Clinical signs of EAE emerged around day 10, peaking at day 14.
Mice exhibited reduced pressure thresholds on days 7 and 10 post-immunization, preceding motor deficits.
The EAE model demonstrated hypernociception prior to the onset of clinical motor impairment.

Conclusions:

The observed hypernociception confirms the MOG35-55 EAE model's utility.
This model is suitable for studying pain mechanisms in the context of multiple sclerosis.