Submitted to: Society for Neuroscience Abstracts and Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/20/2004
Publication Date: 11/20/2004
Citation: Mcguire, S.O., Hejna, M.J., Shukitt Hale, B., Joseph, J.A., Collier, T.J., Lorens, S.A. Dietary supplementation with blueberry extract decreases inflammation after brain injury in rats: implications for neural transplantation. 2004 Society for Neuroscience Abstracts and Proceedings. Interpretive Summary: not needed
Technical Abstract: Reactive gliosis and increased neuroinflammation are common features of multiple types of CNS injury. Since neural transplantation paradigms inadvertently result in CNS injury from needle entry sites, we hypothesized that the resultant gliosis and inflammation might, in part, underlie the poor survival and or efficacy of transplanted dopamine (DA) neurons as a treatment for Parkinson's disease (PD). We have previously shown that dietary supplementation of graft recipients prior to and after grafting with blueberry extract (BBE) improves both the survival and efficacy of transplanted DA neurons in a rat model of PD. In order to determine whether the improvement improvement in transplant outcome was due to an effect at the level of the needle entry site, we examined expression of the gliotic protein, GFAP, and the proinflammatory cytokine, TNF alpha, 4 days after a single needle injury. Young, male F344 rats were fed either a custom formulated rat chow or custom rat chow supplemented with 2% BBE for six weeks. A transplantation needle was introduced sterotaxically into the striatum of anesthetized rats, simulating a DA neuron transplant, and allowed to remain in place for 5 minutes. At 4 days post injury, rats were perfused with ice-cold saline, and striata were removed, dissected on ice and frozen for analysis. Western blotting revealed that the needle entry injury increased expression of GFAP protein in the ipsilateral hemisphere but not in the contralateral hemisphere. Dietary supplementation with BBE suppressed the injury-induced expression of GFAP by 15% (p<0.002). No significant dietary effects were noted for either basal or injury-induced production of TNF alpha.