<img height="1" width="1" style="display:none;" alt="" src="https://px.ads.linkedin.com/collect/?pid=3993628&amp;fmt=gif">

Neural Connections Blog

MD Biosciences insights discussing preclinical research in Pain and Neurodegenerative Conditions

New Publication - A novel sensory wave (p25) in MOG-EAE model

MD Biosciences has published a new article in the Journal of Pain describing a novel sensory wave (P25) in the MOG-induced EAE model

This article assesses p25, a new sensory electrophysiology wave that correlates with pain-related behavior in MOG-induced EAE mice and appears prior to the clinical symptoms. Motor electrophysiology correlates with traditional motor behavior scoring and histology.

Abstract from publication: Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is a murine model for multiple sclerosis. This model is characterized by chronic and progressive demyelination, leading to impairment of motor function and paralysis. While the outcomes of the disease, including impaired motor function and immunological changes, are well- characterized, little is known about the impact of EAE on the electrophysiology of the motor and sensory systems. In this study, we assessed evoked potentials as a quantitative marker for in vivo monitoring of nervous system damage. Motor-evoked potentials (MEPs) and sensory-evoked po- tentials (SEPs) were first standardized in naïve C57BL mice and studied thoroughly in EAE mice. The duration of MEPs and the number of connotative potentials increased significantly alongside an increase in temporal SEP amplitudes. Moreover, a new SEP wave was identified in naïve animals, which significantly increased in MOG-induced EAE animals with no or mild symptoms (clinical score 0–2, 0–5 scale). This wave occurred 25 milliseconds poststimulation, thus named p25. P25 was correlated with increased vocalization and was also reduced in amplitude following treatment with morphine. As the EAE score progressed (clinical score 3–4, 0–5 scale), the amplitude of MEPs and SEPs decreased drastically. Our results demonstrate that desynchronized neural motor activity, along with hypersensitivity in the early stages of EAE, leads to a complete loss of motor and sensory functions in the late stages of the disease. The findings also suggest an increase in p25 amplitude before motor deficits appear, indicating SEP as a predictive marker for disease progression.

View the full article in Journal of Pain. 

Three ways to approach translation

As the general population continues to age, the economic burden of chronic pain and...

electrophysiology: an in vivo biomarker for neurology models

Animal models are commonly used in preclinical development to mimic human disease and response....

Preclinical Human Pain Models. Translating to Clinic

Management of acute pain related to surgical intervention, termed postoperative pain, continues to...

A minipig Model of Incisional pain

The use of animal models for the research of post-operative pain (POP) has been well described[1]....

Do clinical scores tell us all we need to know?

Multiple sclerosis is a disease in which the immune system attacks the myelin sheath that covers...

Assessing and measuring pain behaviors in preclinical studies

Pain plays an important role in human life acting as a defense mechanism that protects us from...

What electrophysiology brings to preclinical studies

Neurons communicate with each other as well as other muscles and organs through electrical events...

Why are potential pain therapies getting lost in translation?

It is estimated that 1.5 billion people worldwide suffer from Chronic pain. While research has seen...