Research Interests


Yohko Hatada  D.Phil


Evolutionary Cognitive Neuroscience


What differentiates living things from non-living things? I am particularly interested in the mechanisms of modifiability by absorbing information from the world as "phenomena of life", using different time scales: adaptive, plastic, developmental and evolutionary mechanisms, and combining between them. I aim to define what the “phenomena of life” are in a unified theory, using different levels from molecular to behavioral interaction within a system and with environmental changes.

For my Masters degree I studied animal behaviour in two nascent different floras (Ecology in M.Sc, University of Durham, UK) and their diversification of life history with comparison to the same species of European continent, as part of evolutionary mechanisms in different environments (including living and non-living environmental factors). For my Ph.D research in Developmental Neuroscience (University of Oxford, UK), I studies evolutionary mechanisms of the core problems of animal-body-form diversification in vertebrate. I asked what is the origin of “organizer”, and how the "organizer" is formed, how the nervous system is induced, the body pattern is defined in chicken ((Hatada and Stern 1994, cited 136) in vertebrates and evolutionary implication (Stern, Hatada et al 1992).  

Then I became focused on the function of the nervous system as most flexible driving force of adaptability, as post-doc and research associate. First, I studied cellular level plasticity in cognitive neurobiology.  I studied the plastic modifiability of neuronal cells in order to understand how neurons in neural networks code and maintain learned memory (Coulumbia University, USA). By studying dynamic live synapse formation in situ, while new synapses were being formed, I studied how synapses are formed under the LTP/ LTF condition in sensory-motor co-culture systems using the exact same cell types with which Aplysia learns to respond to conditional stimuli, and the mechanisms of synapse formation at the molecular level. I found a critically necessary role of rearrangement of cytoskeletal molecules: actin polymerization, for stabilizing memory with synapse formation (Hatada et al 2000, cited 52). Once actin polymerization forms new synapses, the learned memory lasts for days as “late-LTP”. 

Second, utilizing the understanding of plasticity at the cellular or small neural network level, I tried to link the understanding of plasticity at the cellular level to dynamic neural network coding mechanisms within a whole  system by studying how changes due to exposure and interaction with new environments are phenomenologically perceived. In particular, I have been working on the dynamic interaction between various modalities by using adaptation to prism glasses in healthy human. Recently I found a two wave pattern of long lasting aftereffect of prism adaptation. The first wave gradually decayed in hours, becoming non-significant at 6h followed by the second wave which consisted of a late onset of aftereffect one day after the adaptation training and lasted for more than 7 days’ observation without any additional adaptation training (Evaluated in Faculty of 1000 Biology). The clean data is suggestive of e-LTP (early phase of LTP without transcription in nuclei) for the plasticity in the time frame of hours, and l-LTP (late phase of LTP with transcription and synapse formation/neural network modifications) for plasticity over a day (Hatada et al. 2006a). I dissociated biased aftereffects in subcomponents of proprioception depending on the directionality of arm movements (Hatada et al. 2006c).I also found different decay patterns for vision and proprioception aftereffects (Hatada et al. 2006b). From these studies I made a simple model which suggests how changes to the internal egocentric reference frame could develop with a few days’ time delay after the adaptation training (Hatada et al. 2006b, c).  Currently I am extending the research on coding mechanisms of perception of space and time.