KANG Lab - Behavioral Neuropsychopharmacology
Many of the prevalent psychiatric disorders are concomitant with maladaptive reward processing. Understanding how healthy brain mechanisms for context-dependent reward seeking shift into pathological patterns is therefore crucial for making sense of disease-related findings. Our research aims to characterize the exact brain mechanisms responsible for shaping behaviors driven by positive and negative reinforcements.
Our Research Program:
The two overarching questions of our research are like below:
1) How physiological and pathophysiological brain activities that process net-change in positive and negative stimuli shape behavioral outcomes and
2) What are the risk predictable signatures in the related diseases.
Our behavioral neuropsychopharmacology laboratory at UTHealth Houston focuses on several different, but related themes. One of our primary focuses is on a fascinating communication in the brain: the interaction between neurons and astrocytes, a type of non-neuronal glial cell. Accumulative evidence has expanded the known roles of astrocytes beyond structural support, highlighting them as active modulators of neighboring neurons and long-range brain circuits, which functionally work as the critical third partner in synaptic communication. We are working to characterize exactly what these roles look like in both health and disease.
Our ongoing projects to dissect the roles of astrocyte-neuron interaction and identify potential therapeutic targets include:
- Social novelty and autism spectrum disorder (ASD)
- Flexibility in social and non-social reward processing
- Development of alcohol use disorder (AUD) and compulsive drinking
- Neuropsychiatric consequences of repeated ethanol exposure and withdrawal
- Impact of adolescent experience on the behavioral phenotypes in adulthood
- Convergent effects of AUD and alzheimer's disease related dementias (AD/ADRD)
- Cognitive decline in chemobrain, obesity, and hepatic encephalopathy
1) How physiological and pathophysiological brain activities that process net-change in positive and negative stimuli shape behavioral outcomes and
2) What are the risk predictable signatures in the related diseases.
Our behavioral neuropsychopharmacology laboratory at UTHealth Houston focuses on several different, but related themes. One of our primary focuses is on a fascinating communication in the brain: the interaction between neurons and astrocytes, a type of non-neuronal glial cell. Accumulative evidence has expanded the known roles of astrocytes beyond structural support, highlighting them as active modulators of neighboring neurons and long-range brain circuits, which functionally work as the critical third partner in synaptic communication. We are working to characterize exactly what these roles look like in both health and disease.
Our ongoing projects to dissect the roles of astrocyte-neuron interaction and identify potential therapeutic targets include:
- Social novelty and autism spectrum disorder (ASD)
- Flexibility in social and non-social reward processing
- Development of alcohol use disorder (AUD) and compulsive drinking
- Neuropsychiatric consequences of repeated ethanol exposure and withdrawal
- Impact of adolescent experience on the behavioral phenotypes in adulthood
- Convergent effects of AUD and alzheimer's disease related dementias (AD/ADRD)
- Cognitive decline in chemobrain, obesity, and hepatic encephalopathy
To expand our understanding of the cell type-, circuit-, and age-dependent neuropharmacological basis in a variety of related pathologies, our lab applies multi-layered methodological approaches including ex vivo/in vivo electrophysiology, opto/chemo-genetics, viral gene transfer, behavior-synchronized in vivo imaging, spatial 3D reconstruction, and computational analysis.
[Behavior-synced Brain Imaging] [Ex Vivo / In Vivo Electrophysiology] [High-Resolution Imaging - 2D & 3D]
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Upper figure: Evaluation of astrocyte morphology via viral gene transfer. PVT astrocytes labeling by the injections of AAV-GfaABC1D-lck-eGFP / AAV-GFAP-mCherry and Immunofluorescence with signals against S100beta-AF405.