Location: Boston, Massachusetts2009 Annual Report
1a. Objectives (from AD-416)
1: Determine the effects of the radiation on several cognitive and motor behaviors (e.g., Morris water maze), and in addition examine additional new ones (e.g., elevated + maze). 2: Determine whether pre-feeding with Blueberry (BB) or Strawberry (SB) at 2-4% of the diet will prevent the radiation induced deficits in these parameters. 3: We will utilize several techniques (see approach) to assess the changes in several markers of phosphorylation that are important in cell signaling and neurogenesis.
1b. Approach (from AD-416)
The effects of Strawberry (SB) and/or Blueberry (BB) dietary supplementations (8 wks)(control, 2% BB, 2% SB or 1% each SB/BB extracts in the diet for 8 weeks) will be examined in non-irradiated or irradiated (4 mo Sprague Dawley) rats using cognitive and motor tasks. The tests utilized will be age-sensitive motor (inclined screen) and cognitive behaviors (Morris water maze performance, elevated plus maze, sensorimotor gating). We will then determine the effects of the supplementations on neuronal signaling and correlate these with alterations in behavioral parameters determined. We will utilize several techniques (e.g., Western blot analyses and immunocytochemistry) to assess the changes in several markers of phosphorylation that are important in cell communication and neurogenesis (e.g., calcium-dependent protein kinase C, PKC; extracellular signal regulated kinases, ERK).
3. Progress Report
Previous work has shown that exposure to heavy particle irradiation produces neurochemical and cognitive deficits in young animals that are characteristic of much older animals. As a result, it has been suggested that exposure to heavy particles can produce “accelerated aging.” Over the last several years of this project in collaboration with a scientist from UMBC, we have primarily examined the effects of 56Fe irradiation. However, on long-duration missions outside the magnetosphere, astronauts will be exposed to different types of heavy particles, necessitating the evaluation of the neurochemical and behavioral toxicity of other types of heavy particles, such as 16-Oxygen (O). We found that irradiation with 16-O did not affect markers of inflammation or cognition. There were no differences between the groups in hippocampal OX6 expression, a marker of activated microglia, which can cause neuronal damage when in an inflammatory state. Additionally, in the dentate gyrus, there were no differences between the groups in GFAP expression, which is upregulated by astrocytes when they become activated. There were no differences between the groups in spatial learning and memory as measured by both latency to find the platform and probe trial measures such as percent time spent in the platform quadrant and crossings of the previous platform position. These data suggest that 16-O particle irradiation did not increase inflammation or causes deficits in cognitive behavior in rats. However, more studies are needed to establish the effects of higher, or perhaps lower, doses on these and other endpoints, including different markers of inflammation.