Prof. Sang Jeong Kim

Our experience can trigger long-term changes in the strength of the connection between neurons in our brain and this persistent change in neural connections is how the brain stores information such as memory. 

Dr. Sang Jeong Kim focuses on the cellular and molecular mechanisms of information storage and its related brain diseases. In more detail, he explores novel biochemical mechanisms which can understand neural function such as learning and memory and which can also control brain diseases such as pain. 
Cerebellar neural network is his model system to explore mechanisms of memory storage. He explores synaptic plasticity-related function of metabotropic glutamate receptors and transient receptor potential channel proteins in cerebellar Purkinje cells. 

To understand underlying mechanism of clinical situation like pain, he also studies synaptic plasticity in the neural network of spinal dorsal horn which is critical in pain perception. 
He combines cutting-edge techniques such as patch clamping, Ca imaging, confocal microscopy, UV-photolysis and field/single unit recording from isolated neurons, brain slices and in-vivo animals. 
After his efforts and passion in his fields, he has published outstanding papers in major journals such as Nature, Neuron, and Journal of Neuroscience, etc, making over 300 score of the total impact factor during last five years. 

Last year, he has also published a comprehensive review article in Neuron suggesting that ubiquitous synaptic plasticity is necessary to account for the rich phenomenon of memory storage in the neural network. Dr. Kim has joined the editorial board of the Journal of Neurophysiology.




Introduction 

The excitatory synapse is a principal site of information transmission in the brain. The efficacy of synaptic transmission is continuously adjusted through development and lifetime. 

Changes in synaptic efficacy of individual synapses within complex networks of neurons are hypothesized to underlie information storage. These changes are induced in response to neuronal activity associated with information processing and retrieval. 

Signaling by group I mGluRs, which includes mGluR1 and mGluR5 is critical to synaptic circuitry formation during development and is implicated in forms of plasticity such as long?term potentiation (LTP) and long-term depression (LTD) of ionotropic glutamate receptors, such as AMPA receptor (Anwyl, 1999).

At a behavioral level, mGluR1/5 have been implicated in seizure (Wong et al., 1999), addiction (Chiamulera et al., 2001), and several forms of memory storage (Riedel et al., 2003) involving hippocampus, amygdala, neocortex, striatum, and cerebellum. If mGluR1/5 activation were itself modulated, then this might have a metaplastic effect, changing the set point of LTP and LTD induction.



Research topics 

 Cellular and molecular mechanisms of neural plasticity.

 Mechanisms of neural plasticity-related diseases.

 Mechanisms involved in improving learning and memory functions.

 Mechanisms involved in pain regulation.

 Synaptic plasticity related-function of mGluR and TRP proteins in cerebellar Purkinje cells



Prof. Yong-Seok Lee


We are investigating the molecular and cellular mechanism underlying Learning, Memory, and related Disorders such as learning disability, autism, and dementia.


1. Mechanism of learning disability associated with RASopathies (Noonan syndrome).
    RASopathy is a group of developmental disorders caused by the mutations of the genes in Ras-Erk signaling. RASopathy includes Noonan syndrome, NF1, CFC syndrome, Leopard syndrome etc. Cognitive deficits are commonly associated with RASopathy, but the mechanism is largely unknown. We are using mouse models of RASopathy to study the mechanism and treatment for cognitive problems associated with RASopathy. 

2. Molecular & network mechanism of memory enhancement in mice.
    We are searching for the molecular, cellular and network mechanism of memory enhancement that can be used to develop novel treatments for memory disorders including neurodevelopmental and neurodegenerative disorders. 


We are using diverse techniques including 

1. Molecular Biology

2. Mouse Behavior (& optogenetics)

3. Electrophysiology (field recording) 

4. Mutant mice