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Gliopathic Pain: When Satellite Glial Cells Go BadDepartment of Anatomy, University of California, San Francisco, California, peter.ohara{at}ucsf.edu
Department of Anatomy, University of California, San Francisco, California
Department of Surgery, University of California, San Francisco, California
UCLA Headache Research and Treatment Program, David Geffen School of Medicine, University of California, Los Angeles, California
Department of Neurosurgery & Gene Therapeutics Research Institute, Cedars-Sinai Medical Center, Los Angeles, California
UCLA Headache Research and Treatment Program, David Geffen School of Medicine, University of California, Los Angeles, California
Los Angeles Neurosurgical Institute, Beverly Hills, California Neurons in sensory ganglia are surrounded by satellite glial cells (SGCs) that perform similar functions to the glia found in the CNS. When primary sensory neurons are injured, the surrounding SGCs undergo characteristic changes. There is good evidence that the SGCs are not just bystanders to the injury but play an active role in the initiation and maintenance of neuronal changes that underlie neuropathic pain. In this article the authors review the literature on the relationship between SGCs and nociception and present evidence that changes in SGC potassium ion buffering capacity and glutamate recycling can lead to neuropathic pain-like behavior in animal models. The role that SGCs play in the immune responses to injury is also considered. We propose the term gliopathic pain to describe those conditions in which central or peripheral glia are thought to be the principal generators of principal pain generators.
Key Words: trigeminal ganglion • gap junctions • potassium channel • ATP • glutamate recycling
The Neuroscientist, Vol. 15, No. 5,
450-463 (2009) |
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