Description of work

Human choice is constrained by such biological limitations as energetic constraints, sensory limitations, and valuation errors. Our species is not alone in dealing with this dilemma; however, humans seem to have an increased capacity for choice and we struggle to use this capacity on a daily basis. Unfortunately, some people appear to be more constrained than others—for example, individuals afflicted with mental illness or psychiatric disease are extreme cases where human capacity for choice and quality of life is restricted (Kishida, Front Integ Neuro, 2012). While biology imposes limits on human experience and our capacity for choice, we know little about the mechanisms underlying these processes. A research program aimed at these problems promises to make significant advances in determining the biology underlying healthy human cognition; in understanding the processes altered in mental disorders; and, by providing an empirical awareness of the limitations imposed by our neurobiology, in developing effective strategies for alleviating these burdens.

The foundation for my research program is a fundamental interest in determining the neurobiological mechanisms underlying human subjective experience and our capacity for choice. I am particularly interested in discovering heritable “cognitive phenotypes” that have evolved in humans and that drive—or constrain—the choices we make in our modern environments. My approach to this problem begins with a recognition that the psychological narratives we use to depict human mental life have been necessary—but are insufficient—to make headway into determining the neurobiology underlying human cognition. The next step will be the infusion of computational approaches to augment the design and interpretation of experiments probing fundamental aspects of human cognition. My research program integrates quantitative probes of human choice behavior with neurobiological measurement (e.g., functional magnetic resonance imaging and human voltammetry) to generate data that will inform the development of computational models of human subjective experience and capacity for choice. This kind of framework promises to be powerful for revealing deficits underlying mental illness (Kishida et al., Neuron, 2010; Kishida et al., Biol Psych, 2012; Kishida et al., J Neurodev Dis, 2012). Additionally, within this framework, fundamental questions typically handled in the social sciences—such as human narratives, philosophical inquiries, and cultural studies—may be translated and investigated from a computational and biological perspective (Kishida, Front Integ Neuro, 2012; Kishida et al., Phil Trans Roy Soc B, 2012).

Education and Training

• Baylor College of Medicine: Ph.D., Neuroscience
• Baylor College of Medicine: Postdoctoral fellowship

Selected Publications

• Kishida, K.T., Yang, D., Quartz, K.H., Quartz, S.R., and Montague, P.R. (2012). Implicit signals in small group settings and their impact on the expression of cognitive capacity and associated brain responses. Phil. Trans. R. Soc. B, 2012(367):704-16.
• Kishida, K.T. (2012). A computational approach to “free will” constrained by the games we play. Frontiers in Integrative Neuroscience.
• Kishida KT, Li J, Schwind J, Montague PR. (2012). New approaches to investigating social gestures in autism spectrum disorder. Journal of Neurodevelopmental Disorders, 4(14).
• Kishida, K.T., Sandberg, S.S., Lohrenz, T., Comair, Y.G., Saez, I.G., Phillips, P.E.M., and Montague, P.R. (2011). Sub-second dopamine detection in human striatum. PLoS ONE, 6(8):e23291.
• Kishida KT, King-Casas B, Montague PR. (2010). Neuroeconomic approaches to mental disorders. Neuron, 67(4):543-54.
• Chiu PH, Kayali MA, Kishida KT, Tomlin D, Klinger LG, Klinger MR, Montague PR. (2008). Self responses along cingulate cortex reveal quantitative neural phenotype for high-functioning autism. Neuron, 57(3):463-73.
• Kishida KT, Klann E. (2007). Sources and targets of reactive oxygen species in synaptic plasticity and memory. Antioxid Redox Signal, 9(2):233-44.
• Kishida KT, Hoeffer CA, Hu D, Pao M, Holland SM, Klann E. (2006). Synaptic plasticity deficits and mild memory impairments in mouse models of chronic granulomatous disease. Mol Cell Biol, 26(15):5908-20.
• Kishida KT, Pao M, Holland SM, Klann E. (2005). NADPH oxidase is required for NMDA receptor-dependent activation of ERK in hippocampal area CA1. J Neurochem, 94(2):299-306.
• Hoover, K., Kishida, K.T., Digiorgio, L.A., Workman, J., Alaniz, S.A., Hammock, B.D., and Duffey, S.S. (1998). Inhibition of baculoviral disease by plant-mediated peroxidase activity and free radical generation. J. Chem. Ecol:1949-2001.