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Welcome to Dr. Changjoon Justin Lee for Glia-Neuron Interaction.  

Astrocytes are the integral part of the brain and compose the majority of the cell type in the brain. Despite their number and importance, their role has been limited to only supportive function for the neighboring neurons.

In recent years, the role of astrocytes has been re-evaluated and numerous recent reports indicate that these cells are important in many physiological and pathological phenomena. We are particularly interested in their ability to release various transmitters (termed gliotransmitters) including glutamate, d-serine, ATP, GABA, and taurine. Astrocytes appear to actively release various transmitters and communicate dynamically with the neighboring neurons.


In addition, astrocytes wrap each and every synapse by their specialized structure called, microdomain and these microdomains provide structural requirement for close communication between astrocytes and neurons.

In the course of investigating the possible molecular mechanism of the astrocytic release of gliotransmitters, we have found that Ca2+ signaling and Ca2+ dependent channels, in particular, Ca2+ activated anion channels are the critical component of the release machinery.

This is quite contrary to the well known neuronal release mechanism which utilizes vesicular exocytosis machinery. We have obtained compelling evidence that astrocytes utilizes various ion channels, specifically Ca2+ activated anion channels encoded by bestrophin 1 gene, for the release of various gliotransmitters such as GABA and glutamate.

Thus, in addition to studying glia-neuron interaction by gliotransmitters, we also actively investigate the release mechanisms involving anion channels by direct permeation through the channel pore. Finally, we are also quite interested in the question of how G-protein coupled receptors interact with and modulate ion channels. Astrocytes are loaded with various GPCRs that cause Ca2+ increase and changes in cAMP levels. The signaling cascade downstream of GPCRs dynamically controls ion channel functions. The pathological consequences of abnormal GPCR and Ca2+ signaling are evident in the case of glioblastoma cells whose origin is normal astrocytes. In these cells increased expression of GPCR and Ca2+ release channels contribute to the invasiveness and migratory behavior of these cells and the pathogenesis of glioblastoma.

Since September 2004, I have joined the Korea Institute of Science and Technology (KIST), in Seoul Korea, and have been engaged in developing laboratory environment where neuroscientists can communicate freely, formulate creative ideas, and experiment with top-notch instruments.

We employ state-of-the-art technologies to study brain function from multidisciplinary approaches. Anyone who has passion for science and would like to pursue a career in neuroscience is welcome to contact us. This place could be the best place for your career development!

Changjoon Justin Lee, PhD
Principal Investigator
Principal Research Scientist

Director of Center for Neural Science
Deputy Director of Center for Functional Connectomics
Korea Institute of Science and Technology


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Room 7223, Building L7, Division of Life Sciences, KIST, 39-1 Hawolgokdong, Seongbukgu, Seoul, 136-791 Republic of Korea
Tel: +82-2-958-6421 Fax: +82-2-958-6919 E-mail: cjl@kist.re.kr
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