Kuei Y. Tseng, MD, PhD is a Professor in the Department of Anatomy and Cell Biology at the University of Illinois Chicago College of Medicine.
Bio:
My interest in the neurobiology of brain function began in medical school. As a result, I decided to pursue a PhD in neuroscience after obtaining my MD degree. I was a research fellow at the Pitié-Salpêtrière Hospital in Paris. After completing my PhD in Buenos Aires, I continued my neuroscience training the USA. As a neuroscientist with a medical background, I have a long-standing interest in mechanisms of neuronal and non-neuronal forms of plasticity underlying the development of chronic brain disorders. I believe a mechanistic understanding of how a given synaptic function matures and changes during sensitive periods of early postnatal development (e.g., adolescence) through the lifespan and aging is crucial for gaining insight on how brain maladaptive responses emerges and becomes irreversibly abnormal when untreated. In recent years, I have expanded my scientific interests to include two additional research programs: (i) how dysregulation of the serotonin transmission within the meso-corticolimbic circuit triggers the onset of impulsive/disinhibited behavior and maladaptive responses; (ii) how different forms of non-neuronal plasticity converge to sustain abnormal synaptic transmission in neurological syndromes.
Abstract
Exposure to early life adversity (ELA) is known to negatively impact the development of neural circuits controlling threat detection, leading to cognitive and emotional dysregulation later in life. Yet, the underlying mechanisms contributing to such behavioral deficits remain elusive due to our limited understanding of key neural maturation events that are sensitive to ELA. The prefrontal cortex (PFC) is likely to play a pivotal role in driving the circuit-level effects of ELA, given its protracted developmental trajectory and high reactivity to stress. Here I will present unpublished data on how sensitive neuro-developmental processes become vulnerable to the impact of ELA, with emphasis on PFC neural circuits that undergo functional remodeling during the adolescent period. I will then discuss how exposure to ELA at distinct sensitive periods differentially impacts the trajectory of behavioral outcomes and prefrontal circuit maturation from early adolescence through young adulthood. Finally, I will provide examples of chemogenetic approaches to illustrate how cell-type/pathway-specific manipulations at discrete sensitive periods can provide insights on how key corticolimbic circuits are differentially susceptible to the negative impact of ELA