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 aims to elucidate the mechanisms of neurotransmission under various physiological and pathological conditions, with a focus on the prefrontal cortex and hippocampus. By investigating neuronal connectivity, membrane excitability, and learning and memory processes based on intrinsic and synaptic plasticity of neuronal membrane proteins, we study cellular calcium signaling and explore the pathophysiological mechanisms underlying neurological and neuropsychiatric disorders.
Recently, we have developed a cortisol-induced ADHD animal model to investigate the cellular mechanisms underlying memory impairment associated with neurodevelopmental and psychiatric disorders. Through this research, we aim to identify the fundamental causes of neurodevelopmental disorders such as autism and ADHD, and to develop novel therapeutic strategies using endogenous neuroregulators, in collaboration with the KMEDIhub New Drug Development Support Team and the College of Pharmacy.
Our research includes the investigation of neuronal membrane lipids and synaptic connectivity using acute brain slice patch-clamp recordings, as well as studies on prefrontal network specificity using in vivo ensemble recordings. We also analyze the relationship between behavioral phenotypes and cellular mechanisms using various animal models, and examine protein expression levels using Western blotting, ELISA assays, and related techniques.
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 of ADHD induced by prenatal exposure to elevated cortisol levels. This model is expected to cause neuroendocrine dysfunction and dopaminergic dysregulation, thereby affecting neuronal development and contributing to the pathogenesis of ADHD. This model will help elucidate the cellular mechanisms underlying 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 regulate membrane excitability by controlling ionic currents. We focus on A-type K+ channels, which play a key role in action potential firing and postsynaptic responses. Activity-dependent internalization of these channels is essential for synaptic plasticity and excitatory signal processing. Ryanodine receptors in the endoplasmic reticulum also contribute to 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 pathways of the nervous system transmit and process sensory information, including pain. Pain modulation occurs through multiple mechanisms depending on the type of nociceptive input. We investigate the specific roles of TRPA1 channels, which are ROS- and Ca2+-dependent, in pain modulation within primary afferent neurons (dorsal root ganglion neurons).
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Contact
Phone : 064-754-3834/82-64-754-3834
Email : jungsc@jejunu.ac.kr
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