期刊
BRAIN RESEARCH REVIEWS
卷 56, 期 1, 页码 148-169出版社
ELSEVIER
DOI: 10.1016/j.brainresrev.2007.06.006
关键词
neurophatic pain; morphine; tolerance; dependence/withdrawal; interleukin; cytokines; glia; microglia; astrocytes; dorsal root ganglia; peripheral nerves; spinal cord
资金
- NIDA NIH HHS [K02 DA015642-05, R01 DA017670-03, R21 DA015656-02, R01 DA017670, R21 DA015656, K02 DA015642] Funding Source: Medline
- NIDCR NIH HHS [R01 DE017782, R01 DE017782-02] Funding Source: Medline
It is recently become clear that activated immune cells and immune-like glial cells can dramatically alter neuronal function. By increasing neuronal excitability, these non-neuronal cells are now implicated in the creation and maintenance of pathological pain, such as occurs in response to peripheral nerve injury. Such effects are exerted at multiple sites along the pain pathway, including at peripheral nerves, dorsal root ganglia, and spinal cord. In addition, activated glial cells are now recognized as disrupting the pain suppressive effects of opioid drugs and contributing to opioid tolerance and opioid dependence/withdrawal. While this review focuses on regulation of pain and opioid actions, such immune-neuronal interactions are broad in their implications. Such changes in neuronal function would be expected to occur wherever immune-derived substances come in close contact with neurons. (C) 2007 Elsevier B.V. All rights reserved.
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