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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.

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Related Experiment Video

Updated: Dec 17, 2025

Rapid Isolation of Dorsal Root Ganglion Macrophages

Rapid Isolation of Dorsal Root Ganglion Macrophages

Published on: September 7, 2019

Spinal microglia-neuron interactions in chronic pain.

Idy H T Ho^1,2, Matthew T V Chan^1,2, William K K Wu^1,2,3

¹Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Shatin, Hong Kong SAR.

Journal of Leukocyte Biology

|June 24, 2020

Summary

Spinal microglia and neuron interactions are key in pain initiation and chronic pain development. Understanding these neuro-immune changes could lead to new drugs to prevent chronic pain.

Keywords:

acute-to-chronic pain transition microglia microglia-neuronal interactions

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Last Updated: Dec 17, 2025

Rapid Isolation of Dorsal Root Ganglion Macrophages

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Published on: September 7, 2019

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Published on: November 19, 2016

Identifying Microglia and Peripheral Infiltrating Macrophages in the Injured Spinal Cords Using Flow Cytometry

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Published on: June 24, 2025

Area of Science:

Neuroscience
Immunology
Pain Research

Background:

Understanding the transition from acute to chronic pain is crucial for effective treatment development.
Neurocentric mechanisms alone do not fully explain chronic pain, highlighting the importance of neuro-immune interactions.
Spinal microglia, unlike brain microglia, are rapidly activated in pain states, suggesting a key role in pain initiation.

Purpose of the Study:

To review the longitudinal alterations in spinal microglia-neuron interactions during pain hypersensitivity initiation, acute-to-chronic pain progression, and chronic pain maintenance.
To explore the temporal discrepancies in spinal microglia distribution and functions.
To provide insights for developing drugs to prevent the transition of acute pain to chronic pain.

Main Methods:

This is a narrative review.
It summarizes findings from preclinical studies on spinal microglia.
The review analyzes longitudinal alterations in microglia-neuron interactions.

Main Results:

Spinal microglia-neuron interactions are critical for both the initiation and maintenance of pain hypersensitivity.
These interactions involve the release of cytokines, chemokines, and neuroactive substances.
Modulation of synaptic plasticity by microglia-neuron crosstalk plays a significant role in pain.

Conclusions:

Spinal microglia-neuron crosstalk is central to pain initiation and maintenance.
Delineating temporal changes in microglia function offers mechanistic insights for drug development.
Further research into spinal microglia-neuron interactions may yield novel therapeutic strategies for preventing chronic pain.