Abstract
Satellite glial cells (SGCs) undergo phenotypic changes and divide the following injury into a peripheral nerve. Nerve injury, also elicits an immune response and several antigen-presenting cells are found in close proximity to SGCs. Silencing SCG-specific molecules involved in intercellular transport (Connexin 43) or glutamate recycling (glutamine synthase) can dramatically alter nociceptive responses of normal and nerve-injured rats. Transducing SGCs with glutamic acid decarboxylase can produce analgesia in models of trigeminal pain. Taken together these data suggest that SGCs may play a role in the genesis or maintenance of pain and open a range of new possibilities for curing neuropathic pain.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Bromodeoxyuridine / metabolism
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Cell- and Tissue-Based Therapy / methods*
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Connexin 43 / genetics
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Disease Models, Animal
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Ectodysplasins / metabolism
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Facial Pain / therapy
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Gap Junctions / physiology
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Glutamate Synthase / genetics
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Male
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Membrane Cofactor Protein / metabolism
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Models, Biological
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Neuroglia / physiology*
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Pain / etiology*
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Pain Management*
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Pain Measurement / methods
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Peripheral Nervous System Diseases / complications
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RNA, Double-Stranded / therapeutic use
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Rats
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Rats, Sprague-Dawley
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Reward
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Small-Conductance Calcium-Activated Potassium Channels / metabolism
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Trigeminal Ganglion / cytology*
Substances
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Connexin 43
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Ectodysplasins
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Kcnn3 protein, rat
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Membrane Cofactor Protein
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RNA, Double-Stranded
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Small-Conductance Calcium-Activated Potassium Channels
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Glutamate Synthase
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Bromodeoxyuridine