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Name: Masuo Ohno
Title: Research Assistant Professor Degree: Ph.D. Research area: Molecular and Cellular Cognition Address: Department of Physiology Northwestern University Medical School 303 East Chicago Ave. Chicago, IL 60611 Phone: (312) 503-0529 Fax: (312) 503-2090 Email: ohno@northwestern.edu |
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Masuo Ohno |
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Detailed research description: We are studying the mechanisms of learning and memory at system, cellular and molecular levels. Behavioral, biophysical and molecular genetics of the mouse have opened a novel window to explore mechanisms underlying learning and memory, but the major focus of those studies has been on analyzing modifications of synaptic strength (synaptic plasticity, especially hippocampal LTP) with relevance to behavioral plasticity. Our research focuses on understanding molecular constituents and signaling pathways responsible for the modulation of hippocampal neuronal excitability, another important cellular mechanism of learning and memory. Neuronal excitability is primarily determined by the properties of ion channels: K+-channels, in particular, are key components in tuning of the membrane excitability of neurons. Our working hypothesis is that a key molecule required for learning and memory (e.g., CaMKII, etc) not only controls hippocampal synaptic plasticity but also modulates K+-channel properties accounting for an increase in hippocampal neuronal excitability during learning and memory consolidation. Our strategy is the integrated analysis of behavioral, biophysical and biochemical measurements from genetically altered mice. Biophysical recordings from hippocampal slices prepared from the trained mutant and wild-type control mice address a role of a targeted molecule in the mechanisms by which hippocampal neurons are changed in learning temporal (trace eyeblink conditioning) and spatial (water maze) hippocampus-dependent tasks. Importantly, our voltage-clamp analysis isolates and characterizes which components of K+ currents are critical for changing neuronal excitability during hippocampal learning. Further biochemical measurements after learning determine molecular mechanisms and signaling pathways involved in K+-channel-mediated plasticity (e.g., muscarinic activated phosphorylation of K+-channel subunits) which allow hippocampal neurons to be excited enough for processing learning and memory consolidation. For my curriculum vitae please click here 
Selected Publications:
1. Ohno, M., Frankland, P.W., Chen, A.P., Costa, R.M. and Silva, A.J. (2001) Inducible, pharmacogenetic approaches to the study of learning and memory. Nature Neurosci. 4: 1238–1243. 2. Frankland, P.W., O'Brien, C., Ohno, M., Kirkwood, A. and Silva, A.J. (2001) a-CaMKII-dependent plasticity in the cortex is required for permanent memory. Nature 411: 309–313. 3. Costa, R.M., Fedorov, N.B., Kogan, J.H., Murphy, G.G., Stern, J., Ohno, M., Kucherlapati, R., Jacks, T. and Silva, A.J. (2002) Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1. Nature 415: 526–530. 4. Ohno, M., Frankland, P.W. and Silva, A.J. (2002) A pharmacogenetic inducible approach to the study of NMDA/aCaMKII signaling in synaptic plasticity. Curr. Biol., 12: 654-656 (2002). |
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