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Related Experiment Video

Updated: Nov 4, 2025

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

Published on: January 21, 2020

Chronic pain and neuroinflammation.

Pascale Vergne-Salle¹, Philippe Bertin¹

¹Service de rhumatologie, CHU de Dupuytren 2, 16, rue Bernard-Descottes, 87042 Limoges, France.

Joint Bone Spine

|May 22, 2021

Summary

Chronic pain can persist after injury due to central sensitization, a process involving nervous and immune system interactions. This neuroinflammation amplifies pain signals, affecting emotional and cognitive aspects.

Keywords:

Astrocytes Central sensitization Chronic pain Immune system Microglia Neuroinflammation

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Last Updated: Nov 4, 2025

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

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Chronic Constriction of the Sciatic Nerve and Pain Hypersensitivity Testing in Rats

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Development of Recombinant Proteins to Treat Chronic Pain

Development of Recombinant Proteins to Treat Chronic Pain

Published on: April 11, 2018

Area of Science:

Rheumatology
Neuroscience
Immunology

Background:

Chronic pain often arises after musculoskeletal injury, persisting due to central sensitization rather than solely injury progression.
Central sensitization involves complex interactions between the nervous and immune systems, leading to amplified pain signaling.
Peripheral sensitization, linked to inflammation, involves afferent nerve fibers releasing neurotransmitters that activate microglia.

Purpose of the Study:

To describe the pathophysiology of chronic pain.
Incorporate the latest scientific data on neuroplasticity and neuroinflammation in chronic pain.
Explain the mechanisms of central sensitization and neuroinflammation.

Main Methods:

Review of scientific literature on chronic pain pathophysiology.
Analysis of data on nervous and immune system interactions.
Exploration of neuroplasticity and neuroinflammation in pain signaling.

Main Results:

Central sensitization is driven by neuroinflammatory processes initiated by activated microglia.
Neuroinflammation amplifies pain hypersensitivity in second-order neurons.
Neuroinflammation impacts higher brain structures involved in pain modulation and emotional/cognitive processing.

Conclusions:

Central sensitization and neuroinflammation are key mechanisms in chronic pain pathophysiology.
Understanding these processes is crucial for developing effective pain management strategies.
Latest research highlights the intricate interplay between neuroplasticity and neuroinflammation in persistent pain.