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Bong-Kiun Kaang | |
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Born | 1961 (age 62–63) |
Nationality | South Korean |
Alma mater | B.S. Seoul National University (1984) M.S. Seoul National University (1986) Ph.D. Columbia University (1992) Postdoctoral Research Fellow, Center forContentsNeurobiology and Behavior, Columbia University (1992 - 1994) |
Known for | Aplysia, Neuroscience, Learning and Memory |
Awards | Best Research Award, College of Natural Sciences, Seoul National University (2007) Excellent Research Scientist, Korea Ministry of Science and Technology (2007) Life Science Award, Korean Society for Molecular and Cellular Biology (2008) Fellow of the Korean Academy of Science and Technology (2010) |
Scientific career | |
Fields | Neuroscience |
Institutions | Seoul National University, Dept. of Biological Sciences & Brain and Cognitive Sciences |
Doctoral advisor | Eric R. Kandel, M.D.(Nobel Laureate, 2000) |
Kaang Bong-kiun | |
Hangul | 강봉균 |
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Hanja | |
Revised Romanization | Gang Bong-gyun |
McCune–Reischauer | Kang Ponggyun |
Kaang Bong-Kiun was born in Jeju-do,South Korea,on November 21,1961. He is a professor of neuroscience in the Department of Biological Sciences of Seoul National University. He is a Fellow of the Korean Academy of Science and Technology and co-director of the IBS Center for Cognition and Sociality with Changjoon Justin Lee.
He received his bachelor's degree in 1984 and his M.S. in 1986 from the Department of Microbiology,Seoul National University. During his M.S. course,he developed an interest in molecular neuroscience,particularly,in how memory is stored in the brain at the molecular level. He then went to Columbia University where he was supervised by a Nobel laureate Eric R. Kandel for his Ph.D. course and a brief postdoctoral study. He investigated the molecular mechanisms of learning and memory using a simple animal,the marine snail Aplysia. Under the supervision of Dr. Kandel,he received his Ph.D. in 1992. Kaang's Ph.D. thesis,which was entitled,“Studies of Long-Term Facilitation Using Gene Transfer Methods,”introduced the development of the gene delivery system in Aplysia neurons. He continued his research as a postdoctoral research fellow at the Center for Neurobiology and Behavior at Columbia University until 1994,when he was appointed to a faculty position at Seoul National University,Korea.
Kaang's studies have mainly focused on the molecular mechanisms of learning and memory. In his Ph.D. course,he developed the microinjection-based gene transfer method for Aplysia neurons. This technology opened up a new era of molecular studies on the memory mechanisms in Aplysia,as well as of functional studies of receptors,signaling molecules,and ion channels,which play key roles in neuronal functions. He revealed that serotonin-induced transcription requires the protein kinase-A-mediated phosphorylation of the cAMP-response element-binding protein (CREB). Moreover,he found that multiple pulses of serotonin stimulate gene expression that is mediated by the cAMP-response element (CRE). [1] [2]
He continued to study Aplysia when he set up his own laboratory in Korea. He started by establishing an expressed sequence tag database and transcriptome analyses of Aplysia. He identified a serotonin receptor involved in learning-related synaptic facilitation in Aplysia. In addition,he was successful in finding the novel signaling molecules ApLLP,CAMAP,ApPDE4,and ApAUF1,which are involved in long-term facilitation. With his colleagues at Columbia University,he delineated the molecular networks of the molecules that interplay with other regulatory molecules,such as ApCAM,CREB1,CREB2,C/EBP,and ApAF. Furthermore,Kaang reported that,by genetically controlling the expression of these key molecules in specific neurons,he could induce long-term facilitation that lasted days with a single pulse of serotonin that normally induces short-term facilitation that lasts only several minutes. [3] [4] [5] [6] [7] [8] [9] [10] [11]
In parallel with these studies in Aplysia,Kaang has expanded his research field to more complex mammalian models. Combining molecular,electrophysiological,and behavioral experimental tools,he began to explore the mechanisms of learning and memory in mice. One of the major findings from his group was proving the importance of synaptic protein degradation in memory reorganization. He found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after the retrieval of contextual fear memory. Moreover,the infusion of proteasome inhibitors into the CA1 of the hippocampus immediately after retrieval prevented anisomycin-induced memory impairment and the extinction of fear memory. Another major finding from his laboratory was the importance of a kinase,PI3Kγ,in long-term depression and behavioral flexibility. [12] [13] [14]
His interests also include neurological symptoms such as pain and itch and psychiatric disorders,such as autism. One of his major investigations regarding pain was proving that PKMζ,a molecule known for its role in the maintenance of long-term potentiation and long-term memory,is important in maintaining chronic pain in the anterior cingulate cortex. In collaboration with Min Zhuo from the University of Toronto,he showed that the phosphorylation of PKMζwas increased in a neuropathic pain model in the anterior cingulate cortex. In addition,they showed that chronic pain behavior was alleviated by treating mice with the PKMζblocker ZIP,suggesting that this could be a new therapeutic target for treating chronic pain. [15] [16] [17] [18]
In collaboration with M.G. Lee and E. Kim,he demonstrated that NMDAR-dependent synaptic plasticity in the hippocampus is impaired in a mouse model of autism,the Shank2 knockout. When they treated the mice with drugs that upregulate NMDA receptor function,the impairment was recovered,suggesting the possibility that these drugs could be used for treating patients with autism in the future. [19]
Kaang has published 110 research and review articles in a number of journals,including Nature , Science , Cell , Neuron ,and Nature Neuroscience . He has been the editor-in-chief of Molecular Brain . Kaang received the Life Science Award from the Korean Society for Molecular and Cellular Biology in 2008. He was awarded the Donghun Award from the Korean Society for Biochemistry and Molecular Biology in 2012. He also won the Kyung-Ahm Prize in the same year from the Kyung Ahm Foundation.
Eric Richard Kandel is an Austrian-born American medical doctor who specialized in psychiatry,a neuroscientist and a professor of biochemistry and biophysics at the College of Physicians and Surgeons at Columbia University. He was a recipient of the 2000 Nobel Prize in Physiology or Medicine for his research on the physiological basis of memory storage in neurons. He shared the prize with Arvid Carlsson and Paul Greengard.
In neuroscience,long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression,which produces a long-lasting decrease in synaptic strength.
The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor is an ionotropic transmembrane receptor for glutamate (iGluR) that mediates fast synaptic transmission in the central nervous system (CNS). It has been traditionally classified as a non-NMDA-type receptor,along with the kainate receptor. Its name is derived from its ability to be activated by the artificial glutamate analog AMPA. The receptor was first named the "quisqualate receptor" by Watkins and colleagues after a naturally occurring agonist quisqualate and was only later given the label "AMPA receptor" after the selective agonist developed by Tage Honore and colleagues at the Royal Danish School of Pharmacy in Copenhagen. The GRIA2-encoded AMPA receptor ligand binding core was the first glutamate receptor ion channel domain to be crystallized.
In neuroscience,synaptic plasticity is the ability of synapses to strengthen or weaken over time,in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain,synaptic plasticity is one of the important neurochemical foundations of learning and memory.
In neurophysiology,long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
CREB-TF is a cellular transcription factor. It binds to certain DNA sequences called cAMP response elements (CRE),thereby increasing or decreasing the transcription of the genes. CREB was first described in 1987 as a cAMP-responsive transcription factor regulating the somatostatin gene.
Two-hybrid screening is a molecular biology technique used to discover protein–protein interactions (PPIs) and protein–DNA interactions by testing for physical interactions between two proteins or a single protein and a DNA molecule,respectively.
Sensitization is a non-associative learning process in which repeated administration of a stimulus results in the progressive amplification of a response. Sensitization often is characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated. For example,repetition of a painful stimulus may make one more responsive to a loud noise.
Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic,G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad,long-lasting signal. This modulation can last for hundreds of milliseconds to several minutes. Some of the effects of neuromodulators include:altering intrinsic firing activity,increasing or decreasing voltage-dependent currents,altering synaptic efficacy,increasing bursting activity and reconfigurating synaptic connectivity.
Protein kinase C,zeta (PKCζ),also known as PRKCZ,is a protein in humans that is encoded by the PRKCZ gene. The PRKCZ gene encodes at least two alternative transcripts,the full-length PKCζ and an N-terminal truncated form PKMζ. PKMζis thought to be responsible for maintaining long-term memories in the brain. The importance of PKCζin the creation and maintenance of long-term potentiation was first described by Todd Sacktor and his colleagues at the SUNY Downstate Medical Center in 1993.
The cellular transcription factor CREB helps learning and the stabilization and retrieval of fear-based,long-term memories. This is done mainly through its expression in the hippocampus and the amygdala. Studies supporting the role of CREB in cognition include those that knock out the gene,reduce its expression,or overexpress it.
The de novo protein synthesis theory of memory formation is a hypothesis about the formation of the physical correlates of memory in the brain. It is widely accepted that the physiological correlates for memories are stored at the synapse between various neurons. The relative strength of various synapses in a network of neurons form the memory trace,or ‘engram,’though the processes that support this finding are less thoroughly understood. The de novo protein synthesis theory states that the production of proteins is required to initiate and potentially maintain these plastic changes within the brain. It has much support within the neuroscience community,but some critics claim that memories can be made independent of protein synthesis.
Intermediate-term memory (ITM) is a stage of memory distinct from sensory memory,working memory/short-term memory,and long-term memory. While sensory memory persists for several milliseconds,working memory persists for up to thirty seconds,and long-term memory persists from thirty minutes to the end of an individual's life,intermediate-term memory persists for about two to three hours. This overlap in the durations of these memory processes indicates that they occur simultaneously,rather than sequentially. Indeed,intermediate-term facilitation can be produced in the absence of long-term facilitation. However,the boundaries between these forms of memory are not clear-cut,and they can vary depending on the task. Intermediate-term memory is thought to be supported by the parahippocampal cortex.
Alcino J. Silva is a Portuguese-American neuroscientist who was the recipient of the 2008 Order of Prince Henry and elected as a fellow of the American Association for the Advancement of Science in 2013 for his contributions to the molecular cellular cognition of memory,a field he pioneered with the publication of two articles in Science in 1992.
Thomas Carew,dean of the Faculty of Arts and Sciences at New York University,is an American neuroscientist whose interests center on the behavioral,cellular,and molecular analyses of learning and memory. His work provides provide empirical support for the idea that different temporal phases of memory consolidation can be best identified not by their different temporal domains,but by their molecular signatures.
Min Zhuo is a pain neuroscientist at the University of Toronto in Canada. He is the Michael Smith Chair in Neuroscience and Mental Health as well as the Canada Research Chair in Pain and Cognition and a Fellow of the Royal Society of Canada. Zhou was hosted in 2017-2018 as a guest professor at the pharmacology institute at Heidelberg University,Heidelberg.
Priya Rajasethupathy is a neuroscientist and assistant professor at the Rockefeller University,leading the Laboratory of Neural Dynamics and Cognition.
Cristina Maria Alberini is an Italian neuroscientist who studies the biological mechanisms of long-term memory. She is a Professor in Neuroscience at the Center for Neural Science in New York University,and adjunct professor at the Departments of Neuroscience,Psychiatry,and Structural and Chemical Biology at the Icahn School of Medicine at Mount Sinai in New York.
Changjoon Justin Lee is an American neuroscientist specializing in the field of glioscience. He served as the Director of Center for Neuroscience at the Korea Institute of Science and Technology and later founded the WCI Center for Functional Connectomics as part of the World Class Institute Program. In 2015,he established the Center for Glia-Neuron Interaction before becoming co-director of the IBS Center for Cognition and Sociality and head of the Cognitive Glioscience Group in 2018. He has been on the editorial boards of the journals Molecular Brain and Molecular Pain and is a chief editor of Experimental Neurobiology.
Marcello Brunelli was an Italian neurophysiologist and academic.