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Neuroscience. 2014 Aug 22;274:209-17. doi: 10.1016/j.neuroscience.2014.05.029. Epub 2014 May 27.

Systemic inflammation alters satellite glial cell function and structure. A possible contribution to pain.

Author information

1
Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Jerusalem 91240, Israel.
2
Dipartimento di Scienze Biomediche per la Salute, University of Milan, via Mangiagalli 14, I-20133 Milano, Italy.
3
Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Jerusalem 91240, Israel. Electronic address: hananim@cc.huji.ac.il.

Abstract

Local peripheral injury activates satellite glial cells (SGCs) in sensory ganglia, which may contribute to chronic pain. We hypothesized that systemic inflammation affects sensory ganglia like local injury. We induced systemic inflammation in mice by injecting lipopolysaccharide (LPS) intraperitoneally, and characterized SGCs and neurons in dorsal root ganglia (DRG), using dye injection, calcium imaging, electron microscopy (EM), immunohistochemistry, and electrical recordings. Several days post-LPS, SGCs were activated, and dye coupling among SGCs increased 3-4.5-fold. EM showed abnormal growth of SGC processes and the formation of new gap junctions. Sensitivity of SGCs to ATP increased twofold, and neuronal excitability was augmented. Blocking gap junctions reduced pain behavior in LPS-treated mice. Thus, changes in DRG due to systemic inflammation are similar to those due to local injury, which may explain the pain in sickness behavior and in other systemic diseases.

KEYWORDS:

dorsal root ganglion; gap junction; glial activation; purinergic receptors; satellite glial cell; sickness behavior

[Indexed for MEDLINE]

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