Neurology Central

Transcriptional regulation in microglia and neuropathic pain


Microglia are the highly dynamic immune-related glial cells, also known as the specialized tissue macrophage of the CNS [1–3]. Under physiological conditions, these cells are characterized by small cell bodies with actively moving branched processes that survey the surrounding local environment for pathological alterations or disturbances to maintain brain homeostasis [4]. Because microglia have diverse roles during development, infection, aging and neurodegenerative disease [5], they thus exhibit a wide variety of phenotypes, thereby allowing specifically adapted functions, including phagocytosis and synapse remodeling [1,6–7]. Accumulating evidence has also demonstrated the crucial involvement of microglia in the pathogenesis of neuropathic pain [8,9]. In an animal model of neuropathic pain, peripheral nerve injury (PNI), the spinal dorsal horn where the injured nerve projects was found to contain reactive microglia, characterized by their state of morphological hypertrophy and proliferation [8,9]. Furthermore, these cells exhibit dramatic changes in the expression of various genes, including cell-surface receptors for neurotransmission (e.g., nucleotide receptors) and innate responses (e.g., Toll-like receptors), and intracellular signaling molecules and bioactive diffusible factors (e.g., pro-inflammatory cytokines and neurotrophic factors) [1,8].

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