College of Medicine, Jeju National University, South Korea
Cognitive Neurophysiology Lab
인지기능 신경생리 실험실
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Prof. Sung-Cherl Jung, Ph.D
Department of Physiology, College of Medicine
Jeju National University
jungsc@jejunu.ac.kr
Introduction
Our lab strives to realize the characteristics of neurotransmission under various conditions, focusing on the prefrontal cortex and hippocampus. By observing connections between neurons, membrane excitability, and memory learning mechanisms based on substrate and synaptic plasticity of neural membrane proteins, we review calcium signaling of cells and explore the causes and treatment mechanisms of neurological and neuropsychiatric diseases. Recently, a cortisol-induced ADHD animal model has been developed, we are aiming to specify the cause of memory function decline due to neurodevelopmental disorder mental illness at the neuro cell level. Through this research, eventually, we are trying to identify the root causes of neurodevelopmental disorders such as autism and ADHD and to develop new treatments using endogenous neuro regulators, cooperating with the Kmedhub New Drug Development Support Team and the College of Pharmacy.
We are researching the exploration of neuro cellular membrane lipids and connections based on acute brain slice patch clamping, and a study on the specification of prefrontal networking specificity through in-vivo ensemble recording. Also, research on the connection of symptoms and cytological mechanisms through behavioral assessment of various animal models, and the analysis of protein expression level through the Western bot, EISA assay, etc are being conducted now.
Recent Focus Research
Learning and memory mechanism
In mammalian brains, the learning mechanism is based on the synaptic plasticity of the hippocampus inducing memory consolidation. This cellular mechanism is dependent on Ca2+ ions and several types of glutamatergic receptors. We are focusing on the state-dependent characteristics of glutamatergic receptors and cation channels to contribute to the learning and memory mechanism under dynamic pathogenic conditions related to psychological diseases.
Dopaminergic regulation in ADHD and MDD
Our team is developing an animal model with ADHD symptoms induced by prenatal exposure to high cortisol. This experimental protocol supposes to induce neuroendocrine dysfunction and dopaminergic dysregulation, affecting neuronal development and activating the pathogenesis of ADHD. This animal model will help to find cellular mechanisms of neurodevelopmental neuropsychiatric disorders such as ADHD and ASD.
Excitotoxicity and apoptosis in neurons
Most of the neurons in the central nervous system are targeted by dynamic neurotoxic agents and events. Furthermore, endogenous materials such as neurotransmitters, neuromodulators, and ions can also induce neuronal death through neurotoxic regulation. We are focusing on the glutamate- and Ca2+-dependent neurotoxic mechanism in neuronal apoptosis and the related correlation of oxidative stress under various pathogenic conditions.
Membrane excitability regulation of K+ channels
Voltage-dependent ion channels play a role to determine membrane excitability via regulating ionic currents. We are focusing on an A-type K+ channel known as a major ion channel to contribute to action potential firing and postsynaptic responses. Particularly, the activity-dependent internalization of this channel is required for synaptic plasticity and excitable signal processing. Ryanodine receptors in ER are also important to induce K+ channel internalization.
Characterization of Ca2+-permeable glutamatergic receptors
Neuronal excitability is dependent on membrane proteins acting as ion channels and receptors to determine membrane resistance and excitability. Particularly, Ca2+-permeable channels and receptors affect critically neuronal excitability and intracellular signaling. We are focusing on the kinetics of NMDA receptors to dominantly regulate synaptic plasticity and neuronal excitability.
Pain modulation in somatosensory system
The afferent pathway in the nervous system plays a role to transfer and process sensory information. In this pathway, pain is modulated by several steps according to the type of nociception. We are focusing on the specific roles of TRPA1 channels which are ROS- and Ca2-dependent during pain modulation of the primary afferent neuron (DRG neuron).
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Contact
Phone : 064-754-3834/82-64-754-3834
Email : jungsc@jejunu.ac.kr
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