期刊
NEUROSCIENTIST
卷 15, 期 5, 页码 450-463出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1073858409336094
关键词
trigeminal ganglion; gap junctions; potassium channel; ATP; glutamate recycling
资金
- NINDS NIH HHS [R01 NS061241-03, R01 NS061241] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS061241] Funding Source: NIH RePORTER
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.
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