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Il Hwan Kim, PhD

Assistant Professor
Department of Anatomy & Neurobiology

University of Tennessee Health Science Center
855 Monroe Avenue, Link bldg #308
Memphis, TN 38163
Phone: 901.448.2648

Lab homepage:


  • PhD Institution: Korea University, College of Medicine, Department of Anatomy
  • Postdoctoral: Duke University Medical Center, Department of Cell Biology

Research Interests

My research focuses on a fundamental question in neuroscience: “how do at-risk gene mutations lead to neural network dysconnectivity, resulting in behavioral symptoms associated with neuropsychiatric disorders?” To address this question, my lab has been investigating neural circuit and blood-brain barrier (BBB) pathologies that drive endophenotypes associated with neuropsychiatric disorders including schizophrenia (SZ) and autism spectrum disorder (ASD). 


Circuit-level studies for at-risk genes in neuropsychiatric disorders

The central hypothesis of my research is that abnormal behavior is due to perturbations within a common neural circuit, which is shared across different neuropsychiatric disorders driven by various gene mutations. To test this hypothesis, my lab exploits a circuit-specific gene manipulation approach in vivo. Using this innovative method, we knockout/knockin a gene within a neural circuit and investigate the functional characteristics of circuit neurons as well as monitors behavioral phenotypes. We anticipate that our approach will unveil a potential common pathogenic brain network, which drives the behavioral abnormality reported in several mouse models of psychiatric conditions.

Comorbid social dysfunction

“Social Processes” is a major behavioral domain for study in the RDoC Matrix ( Alterations in social behaviors are features of communication disorders, certain anxiety disorders, ASD, and SZ.  Human genetic studies with patients displaying social dysfunction have identified various polymorphisms associated with these abnormalities.  Similarly, a number of different mouse inbred strains as well as genetic models have identified phenotypes that display aberrant social behaviors.  However, with few exceptions the conventional KO mice approach has failed to provide clear mechanistic insights into disorders. Current hypotheses posit that certain genetic mutations may impair the functioning of neural circuits that subserve social behavior.

Gene manipulation within an isolated circuit in vivo

Despite increasing suggestions that a given gene may play a certain role in a specific neural circuit, it has been challenging to demonstrate this point.  My lab has been developing methods for circuit-specific knockout (ctKO) of a given gene and this procedure provides exquisite control in studying genetic effects on neural circuits as they control behavior.  Using this circuit-selective gene manipulation system, we are testing whether genetic abnormalities within a circuit modulate the physiology of circuit neurons and social behaviors.  By incorporating several conditional KO models including ArpC3 and Shank3 floxed lines into this paradigm, we will determine a common circuit pathology for social behavioral deficit. Recently, we found an abnormal circuit function and confirmed social behavioral abnormality in the ArpC3 ctKO mice.

Functional and behavioral assays using circuit-selective expression of transgenes in vivo

My lab also developed a circuit-selective Cre expression system. Using this innovative method, various transgenes including channelrhodopsin 2 (ChR2), halorhodopsin, designer receptors exclusively activated by designer drugs (DREADDs), and the Ca2+-indicator GCaMPs can be exclusively expressed within a defined neural circuit.  This in vivo circuit-specific knockin (ctKI) system is complementary to the ctKO system and it is used for diverse functional assays (in vivo/in vitro electrophysiology, brain endoscope imaging, optogenetics, etc.) targeting a specific neural circuit of interest.  Recently. for example, we selectively expressed GCaMP6 within a defined circuit and verified a functional role of the circuit in social behavior using freely moving mice with brain endoscope.


ASD pathogenesis originating from BBB 

Despite accumulated evidence suggests that ASD is a combined result of genetic and environmental risk factors, we have still limited insights into the gene-environment interaction mechanism that drives the pathogenesis of ASD.  My lab focuses on the non-neuronal compartment, especially brain endothelial cells (BECs) that constitute the Blood-Brain Barrier (BBB) as the most front-line interface between the nervous system and environment.  The overall goal of my study is to uncover the etiological trajectory of ASD development that is originated from ASD-risk gene mutations in BEC/BBB.  My central hypothesis is that ASD-risk gene mutations in the BECs disrupt BBB function, leading to neural network dysconnectivity, resulting in autistic behaviors, which is exacerbated by prenatal stress, one of the most influential environmental risk factors of ASD.  

Using an integrative approach incorporating mouse genetics, proteomics, biochemistry, neurobiological analyses, and behavioral paradigms, we will examine pathogenic processes at multiple levels of analysis to reveal the root cause of ASD originating from BBB.


May 26, 2022