Related Experiment Video
Updated: Oct 10, 2025
Spontaneous and Evoked Measures of Pain in Murine Models of Monoarticular Knee Pain
Published on: February 22, 2019
Complete Freund's adjuvant-induced protein dysregulation correlated with mirror image pain as assessed by
Quan Ma1, Xi Chen2, Jinli Sun3
1School of Life Science and Technology, Harbin Institute of Technology, Harbin, Heilongjiang Province, 150001, China; Department of Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Abstract:
Inflammation or trauma occurring on one side of the body can cause pathological pain on the contralateral noninjured side in a phenomenon called mirror-image pain (MIP). Although some potential mechanisms involved in MIP have been reported, including those involving the immune system and glial cells as well as neural mechanisms, the molecular mechanisms are not well understood. In this study, we aimed to understand the molecular mechanisms in MIP using quantitative proteomics and whole-cell patch clamp recordings. Behavioral test results showed that complete Freund's adjuvant could induce MIP in the mice. The results of isobaric tags for relative and absolute quantification (iTRAQ) quantitative proteomics showed that 108 proteins were dysregulated, and these proteins may represent potential targets. Furthermore, bioinformatics analysis was applied to explore the potential molecular mechanisms during MIP after complete Freund's adjuvant (CFA) treatment. Parallel reaction monitoring (PRM) results showed that PKCδ and seven other dysregulated proteins were related to MIP after CFA treatment. Patch clamp recording results showed that CFA treatment could increase intrinsic excitability and spontaneous firing in spinal cord neurons during MIP. In summary, we found that CFA could induce MIP. The results of proteomic research on the spinal cord after CFA treatment could provide new insight into the molecular mechanisms of MIP. Moreover, the neuronal activity of spinal cord neurons was upregulated during MIP after CFA treatment. In summary, the results of the spinal cord proteomic profile provide a potential molecular mechanism for understanding MIP.
Insights
Inflammation on one side of the body can cause pain on the other side, known as mirror-image pain (MIP). This study used proteomics to identify molecular changes in the spinal cord, revealing potential mechanisms and increased neuronal activity in MIP.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Mirror-image pain (MIP) is pathological pain on the contralateral, non-injured side of the body, triggered by inflammation or trauma on the ipsilateral side.
- While immune, glial, and neural mechanisms are implicated, the precise molecular underpinnings of MIP remain poorly understood.
Purpose of the Study:
- To elucidate the molecular mechanisms of mirror-image pain (MIP) using quantitative proteomics and electrophysiological recordings.
- To identify potential molecular targets for therapeutic intervention in MIP.
Main Methods:
- Induction of MIP in a mouse model using complete Freund's adjuvant (CFA).
- Quantitative proteomics (isobaric tags for relative and absolute quantification - iTRAQ) to analyze spinal cord protein expression.
- Bioinformatics analysis to explore molecular pathways.
- Whole-cell patch clamp recordings to assess neuronal excitability.
- Parallel reaction monitoring (PRM) to validate specific protein changes.
Main Results:
- Complete Freund's adjuvant (CFA) successfully induced mirror-image pain (MIP) in the mouse model.
- Quantitative proteomics identified 108 dysregulated proteins in the spinal cord, including PKCδ, potentially involved in MIP.
- Patch clamp recordings revealed increased intrinsic excitability and spontaneous firing in spinal cord neurons following CFA treatment.
Conclusions:
- CFA-induced MIP provides a valuable model for studying contralateral pain mechanisms.
- Proteomic profiling of the spinal cord offers novel insights into the molecular basis of MIP.
- Upregulated neuronal activity in the spinal cord contributes to the pathophysiology of MIP.
