Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences
Schrift vergrö▀ern Schrift verkleinernBarrierefreie Version
Search | Deutsch
Rhee, Jeong Seop, Dr.


Group leader, Max Planck Institute for Experimental Medicine


  • M.S. in Biology, Sogang University Master thesis, Seoul, Korea (1992)

  • Ph. D. Kyushu University, School of Medicine Department of Physiology, Japan (1997)

  • Assistant Professor, Kyushu University, Faculty School of Medicine Department of Physiology, Japan (1997-2000)

  • Postdoctoral fellow, Max-Planck Institute Biophysical Chemistry, Department of Membranbiophysik, Germany (2000-2004)

  • Assistant Professor, Baylor College of Medicine, Department of Human Genetics and Neuroscience, USA (2004-2006)

  • Group Leader, Max Planck Institute of Experimental Medicine, Göttingen, Germany (since 2006)



Major Research Interests

Neurophysiology Group

We study that signaling between nerve cells in the brain is mainly mediated at synapses, which are specialized cellular contact sites. The transfer of information at synapses can be regulated dynamically, a process that is called synaptic plasticity. Our main research goal is to elucidate the molecular mechanisms that underlie synaptic plasticity at synapses in the central nervous system. For this purpose we mainly use electrophysiological methods, in combination with nerve cells from genetically modified mice or virus-mediated molecular perturbation of nerve cell function.

Neurotransmitter release is the first step in synaptic signaling. It is mediated by exocytosis of synaptic vesicles at highly specialized contact sites, the active zones of synapses. Neurotransmitters are stored in synaptic vesicles, which undergo a complex trafficking cycle in the presynaptic compartment in order to sustain the rapid and repetitive transfer of information between nerve cells. Synaptic vesicles are initially tethered at the active zone plasma membrane, a process termed docking. Subsequently vesicles undergo a prefusion reaction termed priming, which renders docked vesicles fusion competent, thus defining the readily releasable pool of vesicles. Triggered by the arrival of an action potential at the nerve terminal and the concomitant increase in the intracellular Ca2+ concentration, a fraction of fusion competent vesicles in the readily releasable pool fuse with the plasma membrane and release their content. After fusion, vesicular membrane and protein components are recycled by endocytosis and used for additional rounds of exocytosis.

Essentially, each step of the synaptic vesicle cycle can contribute to the regulation of synaptic plasticity. We combine mouse genetics, molecular biological and morphological methods, and patch clamp electrophysiological analyses of autaptic cultured neurons, organotyptic brain slice cultures, acute brain slices, or acutely isolated neurons with active presynaptic terminals in order to identify the molecular mechanisms underlying the individual synaptic vesicle recycling steps. In the past, we characterized mutant mice lacking identified presynaptic protein components of the neurotransmitter release machinery. Experiments on mutant mouse neurons are complemented by virus mediated expression of proteins in cultured neurons, which allows us to perform detailed structure-function analyses of presynaptic proteins.



Selected Recent Publications


  • Wojcik SM, Katsurabayashi S, Guillemin I, Friauf E, Rosenmund C, Brose N, Rhee JS* (2006). A Shared Vesicular Carrier Allows Synaptic Corelease of GABA and Glycine. Neuron 50: 575-87

  • Adamcio B, Sargin D, Stradomska A, Medrihan L, Gertler C, Theis F, Zhang M, Muller M, Hassouna I, Hannke K, Sperling S, Radyushkin K, El-Kordi A, Schulze L, Ronnenberg A, Wolf F, Brose N, Rhee JS, Zhang W, Ehrenreich H. (2008). Erythropoietin enhances hippocampal long-term potentiation and memory. BMC Biol 6:37.

  • Jockusch W, Speidel D, Sigler A, S°rensen J, Varoqueaux F, Rhee JS*, Brose N* (2007). CAPS-1 and CAPS-2 are essential synaptic vesicle priming proteins. Cell 131:796-808.

  • Shin OH, Lu J, Rhee JS, Tomchick DR, Pang ZP, Wojcik SM, Camacho-Perez M, Brose N, Machius M, Rizo J, Rosenmund C, Südhof TC. (2010). Munc13 C(2)B domain is an activity-dependent Ca(2+) regulator of synaptic exocytosis. Nat Struct Mol Biol. 17: 280-288.
  • Kawabe H*, Neeb A, Dimova K, Young SM Jr, Takeda M, Katsurabayashi S, Mitkovski M, Malakhova OA, Zhang DE, Umikawa M, Kariya K, Goebbels S, Nave KA, Rosenmund C, Jahn O, Rhee JS, Brose N*. (2010) Regulation of Rap2A by the ubiquitin ligase Nedd4-1 controls neurite development in cortical neurons. Neuron 65:358-372.

  • Wojcik SM, Katsurabayashi S, Guillemin I, Friauf E, Rosenmund C, Brose N, Rhee JS. (2006). A Shared Vesicular Carrier Allows Synaptic Corelease of GABA and Glycine. Neuron 50(4):575-87


  • *joint corresponding authors







    Rhee, Jeong Seop

    Address

    Dr. Jeong Seop Rhee
    Max Planck Institute for Experimental Medicine
    Neurophysiology Group
    Hermann-Rein-Str. 3
    37075 Göttingen
    Germany

    Tel.: +49-(0)551-38 99694
    Fax: +49-(0)551-38 99715
    e-mail: rhee@em.mpg.de

    GGNB Affiliation
    Sensory and Motor Neuroscience
    Neurosciences (IMPRS)