Abstract
Chronic pain is a worldwide refractory health disease that causes major financial and emotional burdens and that is devastating for individuals and society. One primary source of pain is inflammation. Current treatments for inflammatory pain are weakly effective, although they usually replace analgesics, such as opioids and non-steroidal anti-inflammatory drugs, which display serious side effects. Emerging evidence indicates that the membrane G protein-coupled estrogen receptor (GPER) may play an important role in the regulation of inflammation and pain. Herein, we focus on the consequences of pharmacological and genetic GPER modulation in different animal models of inflammatory pain. We also provide a brief overview of the putative mechanisms including the direct action of GPER on pain transmission and inflammation.
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