Low dose ionizing radiation exposure can alter unmotivated mouse behavior and brain-based inflammatory mediators (116.34)

Abstract

Abstract Individuals exposed to ionizing radiation (IR) experience acute radiation syndrome, the prodromal phase of which includes symptoms such as malaise and fatigue. These symptoms and related adverse biobehaviors have mental, physical and motivational elements that can be difficult to experimentally isolate. We’ve developed an experimental system to test IR-induced fatigue in mice using gamma rays to deliver total body IR in both motivated and unmotivated settings. 6h after a 50cGy dose of 137Cs whole body radiation, mice had a 34% reduction in spontaneous distance moved and average velocity of movement compared to non-irradiated mice. In contrast, the motivated behavior social exploration of a novel juvenile showed non-statistically significant trends toward reduced activity up to 6h post-IR. Examination of brain-based immunity showed whole brain TNF-α mRNA was significantly increased at 4 and 6h post-IR and this increase was coupled to 1) an up-regulation of IL-1RA and down-regulation of IL-6 mRNAs 4h post-IR and 2) a down-regulation of IL-1β, IFN-γ and F4/80 mRNAs at 6h post-IR. Together these data show that shortly after low-dose IR, mouse activity is reduced but can be overcome via a motivator. This altered locomotion is tied to a brain-based alteration in pro/anti-inflammatory balance. These data suggest anti-inflammatory therapies such as corticosteroids or anti-TNF/IL-1 agents may be effective countermeasures for prodromal symptoms due to IR exposure.