We report results from an exploratory study using eye-tracking recording of information acquisition by players in a game theoretic learning paradigm. Eye-tracking is used to observe what information subjects look at in 4x4 normal-form games; the eye-tracking results favor sophisticated learning over adaptive learning and lend support to anticipatory or sophisticated models of learning in which subjects look at payoffs of other players to anticipate what those players might do. The decision data, however, are poorly fit by the simple anticipatory models we examine. We discuss how eye-tracking studies of information acquisition can fit into research agenda seeking to understand complex strategic behavior and consider methodological issues that must be addressed in order to maximize their potential.
Hypersensitivity to oxygen and shortened lifespan in a Drosophila mitochondrial complex II mutant
D. W. Walker and P. Hajek and J. Muffat and D. Knoepfle and S. Cornelison and G. Attardi and S. Benzer
Proceedings of the National Academy of Sciences of the United States of America
Oxidative stress is implicated as a major cause of aging and age-related diseases, such as Parkinson's and Alzheimer's, as well as ischemia-reperfusion injury in stroke. The mitochondrial electron transport chain is the principal source of reactive oxygen species within cells. Despite considerable medical interest, the molecular mechanisms that regulate reactive oxygen species formation within the mitochondrion remain poorly understood. Here, we report the isolation and characterization of a Drosophila mutant with a defect in subunit b of succinate dehydrogenase (SDH; mitochondrial complex II). The sdhB mutant is hypersensitive to oxygen and displays hallmarks of a progeroid syndrome, including early-onset mortality and age-related behavioral decay. Pathological analysis of the flight muscle, which is amongst the most highly energetic tissues in the animal kingdom, reveals structural abnormalities in the mitochondria. Biochemical analysis shows that, in the mutant, there is a complex II-specific respiratory defect and impaired complex II-mediated electron transport, although the other respiratory complexes remain functionally intact. The complex II defect is associated with an increased level of mitochondrial hydrogen peroxide production, suggesting a possible mechanism for the observed sensitivity to elevated oxygen concentration and the decreased lifespan of the mutant fly.