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Satellite glial cells in the trigeminal ganglion as a determinant of orofacial neuropathic pain

Published online by Cambridge University Press:  13 April 2007

Jean-Philippe Vit
Affiliation:
Department of Anatomy, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0485, USA Department of Neurosurgery and Gene Therapeutics, Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Davis Building Research Pavilion, Room 5090, Los Angeles, CA 90048, USA
Luc Jasmin*
Affiliation:
Department of Anatomy, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0485, USA Department of Neurosurgery and Gene Therapeutics, Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Davis Building Research Pavilion, Room 5090, Los Angeles, CA 90048, USA
Aditi Bhargava
Affiliation:
Department of Surgery, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0660, USA
Peter T. Ohara
Affiliation:
Department of Anatomy, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0485, USA
*
Correspondence should be addressed to Luc Jasmin, Department of Anatomy, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0485, USA phone: 310-423-7338, fax: 310-423-7308 email: [email protected]

Abstract

Satellite glial cells (SGCs) tightly envelop the perikarya of primary sensory neurons in peripheral ganglion and are identified by their morphology and the presence of proteins not found in ganglion neurons. These SGC-unique proteins include the inwardly rectifying K+ channel Kir4.1, the connexin-43 (Cx43) subunit of gap junctions, the purinergic receptor P2Y4 and soluble guanylate cyclase. We also present evidence that the small-conductance Ca2+-activated K+ channel SK3 is present only in SGCs and that SGCs divide following nerve injury. All the above proteins are involved, either directly or indirectly, in potassium ion (K+) buffering and, thus, can influence the level of neuronal excitability, which, in turn, has been associated with neuropathic pain conditions. We used in vivo RNA interference to reduce the expression of Cx43 (present only in SGCs) in the rat trigeminal ganglion and show that this results in the development of spontaneous pain behavior. The pain behavior is present only when Cx43 is reduced and returns to normal when Cx43 concentrations are restored. This finding shows that perturbation of a single SGC-specific protein is sufficient to induce pain responses and demonstrates the importance of PNS glial cell activity in the pathophysiology of neuropathic pain.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2007

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