Effects of social defeat on iK-ba inflammatory signaling in male c57BL/6J

Abstract

An estimated 30 million people in the United States have been diagnosed with mood and anxiety disorders. Unfortunately, many of these patients do not adequately respond to current pharmacotherapies, so developing new drugs and strategies to treat such disorders is critically important. There are only a few drugs on the market that target neuroinflammation. Thus, it's critical that we identify anti-inflammatory agents that effectively reduce neuroinflammatory responses, hereby expanding or augmenting available options for treating neurological disorders. Previous work has shown that the derivative of naltrexone, B-funaltrexamine (B-FNA), inhibits inflammatory signaling in human astrocytes in reduced expression of proinflammatory chemokines. IKBa is one of the specific signaling proteins in the inflammation pathway.