The Effect of Inhibiting IL-1β Release on Fear Aquisition and Fear Memory 

https://kent-islandora.s3.us-east-2.amazonaws.com/node/10349/10495-thumbnail.jpgChronic stress induces anxiety-like behaviors, including contextual fear memory. In the presence of stress, microglia, the immune cells of the brain, release the proinflammatory cytokine interleukin-1β (IL-1β). Previous studies have demonstrated that a slight increase in IL-1β can enhance fear memory in rats. However, an excess or lack of IL-1β can dampen fear memory. This study sought to examine the role of IL-1β on fear acquisition and fear memory under chronic stress conditions. To do so, the effect of the drug minocycline on this pathway was investigated. Minocycline has been previously demonstrated to inhibit microglial activation, thus halting release of IL-1β. This investigation hypothesized that minocycline administration in stressed rats would result in dampened fear memory. Rats were separated into stress and no-stress groups, then were either administered minocycline or saline 1h prior to fear conditioning. In conditioning, fear acquisition was measured and analyzed. The data suggest memory acquisition was intact. Additionally, there was a significant interaction of time and chronic stress in which chronic stress enhances fear acquisition. Fear memory was analyzed 24h post fear conditioning by measuring freezing behavior in the same context. Unexpectedly, results show no significant effect of chronic stress or a significant interaction of chronic stress and minocycline on fear memory. However, the data suggest minocycline significantly dampens contextual fear memory in rats. Previous studies have shown that increased IL-1β in the basolateral amygdala (BLA) results in dampened fear memory. Thus, future studies will further investigate effects of inhibiting IL-1β release in the BLA