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Systemic inflammation alters satellite glial cell function and structure. A possible contribution to pain
E Blum1, P Procacci2, V Conte2
1Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Jerusalem 91240, Israel.
Systemic inflammation, like local injury, activates glial cells in sensory ganglia. This activation increases neuronal excitability and pain, suggesting a link between inflammation and chronic pain conditions.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Local peripheral injury activates satellite glial cells (SGCs) in sensory ganglia, potentially contributing to chronic pain.
- The effect of systemic inflammation on sensory ganglia remains less understood.
Purpose of the Study:
- To investigate whether systemic inflammation affects sensory ganglia similarly to local injury.
- To characterize the changes in SGCs and neurons in dorsal root ganglia (DRG) following systemic inflammation.
Main Methods:
- Systemic inflammation induced in mice via intraperitoneal lipopolysaccharide (LPS) injection.
- Characterization of SGCs and neurons using dye injection, calcium imaging, electron microscopy (EM), immunohistochemistry, and electrical recordings.
- Assessment of pain behavior and the effect of gap junction blockade.
Main Results:
- LPS induced SGC activation and increased SGC dye coupling 3-4.5-fold.
- EM revealed abnormal SGC process growth and new gap junction formation.
- Increased SGC sensitivity to ATP, augmented neuronal excitability, and reduced pain behavior upon gap junction blockade were observed.
Conclusions:
- Systemic inflammation induces changes in DRG similar to local injury.
- These DRG changes, including SGC activation and altered neuronal excitability, may explain pain associated with systemic inflammation and disease.
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