Home ＞GCOE Researchers ＞Yoichi ODA

GCOE Researchers

Yoichi ODA

Affiliation
/Position		 Graduate School of Science, Division of Biological Science, Professor
Doctorate Doctor of Engineering
Research interests Principle of brain function and organization
address oda＠bio.nagoya-u.ac.jp
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+81-52-789-2978
  Laboratory

Outline of research

We get information from the outside world via a variety of senses based on sensory information, and generate motor command signals to move our body. What is the basis of the brain’s wondrous ability to process information? Within the human brain, hundreds of billions of neurons are involved in neural networks that process the sensory and motor signals. Although the brain appears very complicated, this complexity is a consequence of evolution. Therefore, we think that the principle of the brain function is based on the principle of the brain organization and modification of function is associated with evolutional change in the organization. We set ourselves the goal of understanding the fundamental mechanisms of sophisticated brain functions, using zebrafish and C. elegans as model systems for our research.

One of our research topics is a hindbrain circuit which controls escape behavior in zebrafish. The escape behavior, by which animals evade from enemies and avoid nociceptive stimuli, is a fundamental behavior for ensuring individual survival. Furthermore, two essential functions of the brain - the integration of sensory information and the generation of suitable behavioral output - are combined in this behavior. In teleosts such as zebrafish, Mauthner (M) cells, which is differentiate to neuron first in the hindbrain, initiate the escape behavior. M cells receive sensory input directly at their dendrites and send an axon to the spinal cord to deliver output to contract the trunk muscles along the contralateral side of body. In addition to M cell, homologous neurons in the hindbrain that have developmental and morphological characteristics similar to those of M cells also play important roles in the control of escape behavior. To understand how the circuit that produces the signals for quick escape in the hindbrain neurons is constructed and functionally matured, we are conducting a wide range of research. Our studies include thorough analysis of escape behavior, patch clamp recording and calcium imaging of the neurons, and screening for expression of channel molecules that generate the circuit function. For these analyses, we are making use of transgenic zebrafish that express fluorescent proteins in specific neurons. Also, using zebrafish mutants defective in normal escape behavior, we are identifying responsible genes, analyzing expression and physiological functions of proteins, and examining roles in motor control of the proteins. Because these mutants can be model systems for motor disorders, we expect that our work will be applied to both the understanding and treatment of disorders in humans.
To construct elaborate neural circuit, neurons need to be connected to each other correctly. We have undertaken studies of a signal molecule called semaphorin, which controls axon extension, and its receptor, plexin, in vertebrates. We anticipate that the resulting findings will be useful in the elucidation of the mechanism of neural-circuit formation and nerve-fiber regeneration. We are also studying the roles of those molecules in intracellular signal transduction in development, using C. elegans as a model organism.

References

  1. Kohashi T., & Oda Y. (2008) Initiation of Mauthner- or non-Mauthner-mediated fast escape evoked by different modes of sensory input. J. Neurosci., 28: 10641-10653.
  2. Nukazuka A. et al. (2008) Semaphorin controls epidermal morphogenesis by stimulating mRNA translation via eIF2alpha in Caenorhabditis elegans. Genes Dev., 22: 955-999.
  3. Hirata H. et al. (2007) Zebrafish relatively-relaxed mutants have a ryanodine receptor defect, show slow swimming and provide a model of multi-minicore disease Zebrafish. Development, 134: 2771-2781.
  4. Nakao F. et al. (2007) The plexin PLX-2 and the ephrin EFN-4 have distinct roles in MAB-20/Semaphorin 2A signaling in C. elegans morphogenesis. Genetics, 176: 1591-1607.
  5. Hirata H. et al. (2005) Zebrafish bandoneon mutants display behavioral defects due to a mutation in the glycine receptor beta subunit. Proc. Natl. Acad. Sci. USA, 102: 8345-8350.
  6. Liu Z. et al. (2005) C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in vulval precursor cells. Dev. Biol., 282: 138-151.
  7. Nakayama H., & Oda Y. (2004) Common inputs and different excitability of segmentally homologous reticulospinal neurons in hindbrain. J. Neurosci., 24: 3199-3209.
  8. Hirata H. et al. (2004) accordion, a zebrafish behavioral mutant, has a muscle relaxation defect due to a mutation in the ATPase calcium pump SERCA1. Development, 131: 5457-5468.
  9. Fujii T. et al. (2002) Caenorhabditis elegans PlexinA, PLX-1, interacts with transmembrane semaphorins and regulates epidermal morphogenesis. Development, 129: 2053-2063.
  10. Takahashi, M. et al. (2002) In vivo imaging of functional inhibitory networks on the Mauthner cell of larval zebrafish. J. Neurosci., 22: 3929-393.

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