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Cognitive Learning and Dynamics Laboratory

Ain Chung

Assistant Professor

Prior cognitive experiences impact our ability to learn new information. Particularly, early life experiences significantly affect cognitive function in adulthood. The prevailing synaptic plasticity and memory hypothesis suggests that brain circuits undergo activity-dependent synaptic plasticity to update memories and facilitate these adaptive learning processes. The current evidence for this hypothesis does not yet explain how brain circuits adapt over long timescales, as is the case when early life experiences impact cognition in adulthood. The Cognitive Learning and Dynamics Laboratory (CoLD Lab) will try to fill this critical knowledge gap by investigating the neurobiological mechanisms underlying long-lasting and flexible changes in cognition by salient life experiences.
The research outcomes will advance our knowledge of neural mechanisms underlying persistent cognitive function changes by adolescent social experience. Neurogenesis-dependent inhibitory plasticity may serve as a potential therapeutic target for improving impaired cognition after early social stress. In addition, uncovering the neurobiological link between adolescent social stress and impaired learning will be informative for adolescent education and psychological assessment. Since cognitive control training is widely used to strengthen cognitive and emotional functions in cognitive behavioral therapy (CBT), researches in CoLD lab harbor the potential to impact the development of clinical interventions for neuropsychiatric and behavioral disorders. Furthermore, circuit-level understanding of how the brain achieves cognitive flexibility and learning to learn will also inspire innovative brain-inspired AI solutions.

Research Areas 1) Changes in large scale inhibitory plasticity, brain synchrony and cognitive function after the early experience.

2) The link between inhibition alteration and the learning set formation/refinement.

3) Inhibitory plasticity responsibilities in cognitive deficit rescues.

Research Area 1) Early life cognitive experience, global inhibitory interneuron plasticity and cognitive function.

The adolescent brain is characterized by functional flexibility and structural sensitivity. Compared to the adult brain, the teenage brain shows a significantly higher level of neurogenesis, which is vulnerable to social stress. Social stress decreases hippocampal neurogenesis and impairs social cognition. Anatomical studies demonstrated that specific inhibitory synapses onto pyramidal neurons in the hippocampus and prefrontal cortex strengthen in adolescence. Adolescent social stress decreases neurogenesis leading to persistent deficits in spatial memory and social cognition. My research program will study how social/cognitive experience in adolescents regulates neurogenesis-dependent neuronal plasticity and brain synchrony leading to impaired cognitive functions.

Research Area 2) Neural network mechanisms underlying cognitive flexibility and learning to learn.

Although there is an increasing demand for understanding neural mechanisms underlying human cognitive flexibility and learning efficiency, there is a lack of circuit-level investigation on how the brain achieves cognitive flexibility and learning to learn. Cognitive training induces learning to learn in mice and increases the long-term potentiation marker in the hippocampus in a compartment-specific way. During cognitive task, transient increased excitatory-inhibitory coupling was observed in the hippocampus when cognitive demand is elevated, the same cognitive task induced persistent hippocampal inhibition changes. Despite of evidence that inhibitory interneurons are critically engaged in cognitive control and memory acquisition process, there is a lack of knowledge on how INs are engaged in cognitive control learning, in compartment-specific and cell type specific way. Therefore, my research program will aim to model the relationship between dynamic plastic changes in various circuit function changes and persistent cognitive enhancement.

Research Area 3) Enhancing synaptic plasticity to rescue cognitive function

Increased neurogenesis was shown to enhance memory discrimination or rescue cognitive impairment in aged animals. Cognitive control training strengthened inhibitory circuit function in the hippocampus and rescued impaired cognitive function in mice and human. Social enrichment in early life rescued impaired cognition in the autism mouse model. Social enrichment can reverse neuronal plasticity deficits caused by adolescent social stress, which requires adult neurogenesis. Moreover, adolescent exposure to the enriched environment or induced inhibitory synaptic plasticity in the hippocampus rescued the mouse's cognitive function. However, it is unclear whether inhibitory plasticity is necessary and sufficient to reverse cognitive impairment by early life stress. My research program will study whether increased inhibitory plasticity reverses the social isolation effects on circuit function and social behaviors.