Interleukin-1 α in the ventral hippocampus increases stress vulnerability and inflammation-related processes.

Interleukin-1α in the ventral hippocampus increases stress vulnerability and inflammation-related processes.
Stress. 2019 Sep 27;:1-34
Authors: Pearson-Leary J, Eacret D, Bhatnagar S
Abstract
Mechanisms of stress vulnerability remain elusive. Previous research demonstrated that inflammation-related processes in the brain play a role in stress vulnerability. Our previous research showed that inflammatory processes in the ventral hippocampus (vHPC) induced a stress vulnerable phenotype. To further understand neuroinflammatory processes in the vHPC in stressed rats, we determined that protein levels of the pro-inflammatory cytokine interleukin-1-α (IL-1α), but not interleukin-1β (IL-1β), were increased in the vHPC of rats vulnerable to the effects of repeated social defeat compared to rats resilient to its effects. Injections of IL-1α into the vHPC increased stress vulnerability as characterized by increases in passive coping during defeat and subsequent decreased social interactions. Conversely, injections of recombinant IL-1 receptor antagonist (IL1-RA) increased latencies to social defeat and decreased anxiety-like behaviors during social interaction, suggesting an reduction in stress vulnerability. Protein analyses revealed increased FosB expression in the vHPC of IL-1α-injected rats, and increased HPA activation following a social encounter. Further analysis of vHPC of IL1-α-injected rats showed increased density of microgl...

Source: Stress - September 29, 2019 Category: Research Tags: Stress Source Type: research