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. 2012 Apr;12(2):41-7.
doi: 10.4110/in.2012.12.2.41. Epub 2012 Apr 30.

Glia as a Link between Neuroinflammation and Neuropathic Pain

Mithilesh Kumar Jha  1 , Sangmin Jeon, Kyoungho Suk
Affiliations

Glia as a Link between Neuroinflammation and Neuropathic Pain

Mithilesh Kumar Jha et al. Immune Netw. 2012 Apr.

Abstract

Contemporary studies illustrate that peripheral injuries activate glial components of the peripheral and central cellular circuitry. The subsequent release of glial stressors or activating signals contributes to neuropathic pain and neuroinflammation. Recent studies document the importance of glia in the development and persistence of neuropathic pain and neuroinflammation as a connecting link, thereby focusing attention on the glial pathology as the general underlying factor in essentially all age-related neurodegenerative diseases. There is wide agreement that excessive glial activation is a key process in nervous system disorders involving the release of strong pro-inflammatory cytokines, which can trigger worsening of multiple disease states. This review will briefly discuss the recent findings that have shed light on the molecular and cellular mechanisms of glia as a connecting link between neuropathic pain and neuroinflammation.

Keywords: Astrocyte; Glial activation; Microglia; Neuroinflammation; Pain.

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Conflict of interest statement

The authors have no financial conflict of interest.

Figures

Figure 1
Figure 1
Diagram showing the neuroinflammation and neuropathic pain subsequent to the neuronal injury and glial cell (microglial and astrocytic) activation. Following a peripheral injury, the synaptic projection of pain sensing neuron within the spinal cord releases ATP. Nearby microglial cells are drawn to the source of ATP and undergo morphological changes as they approach the source and become activated. Fully activated microglial cells are localized around the pain sensing neuron and begin to interact with the neurons at a molecular level, releasing various neuroinflammatory agents. These neuroinflammatory agents activate astrocytes. Upon activation, the astrocytes undergo hypertrophy and increased production of neuroinflammatory agents are secreted into the synaptic cleft. Astrocyte activation in conjugation with microglial activation significantly depolarizes the neuron increasing its sensitivity and potentiating the neuroinflammation and neuropathic pain states. EAA, excitatory amino acids.
See this image and copyright information in PMC

References

    1. Kriegstein A, Alvarez-Buylla A. The glial nature of embryonic and adult neural stem cells. Annu Rev Neurosci. 2009;32:149–184. - PMC - PubMed
    1. Moalem G, Tracey DJ. Immune and inflammatory mechanisms in neuropathic pain. Brain Res Rev. 2006;51:240–264. - PubMed
    1. Aamodt S. Focus on glia and disease. Nat Neurosci. 2007;10:1349. - PubMed
    1. Watkins LR, Milligan ED, Maier SF. Glial activation: a driving force for pathological pain. Trends Neurosci. 2001;24:450–455. - PubMed
    1. McMahon SB, Cafferty WB, Marchand F. Immune and glial cell factors as pain mediators and modulators. Exp Neurol. 2005;192:444–462. - PubMed