Recent years have seen a considerable surge of research on interest-based engagement, examining how and why people are engaged in activities without relying on extrinsic rewards. However, the field of inquiry has been somewhat segregated into three different research traditions which have been developed relatively independently --- research on curiosity, interest, and trait curiosity/interest. The current talk sets out an integrative perspective; the reward-learning framework of knowledge acquisition. This conceptual framework takes on the basic premise of existing reward-learning models of information seeking: that knowledge acquisition serves as an inherent reward, which reinforces people’s information-seeking behavior through a reward-learning process. However, the framework reveals how the knowledge-acquisition process is sustained and boosted over a long period of time in real-life settings, allowing us to integrate the different research traditions within reward-learning models. The framework also characterizes the knowledge-acquisition process with four distinct features that are not present in the reward-learning process with extrinsic rewards --- (1) cumulativeness, (2) selectivity, (3) vulnerability, and (4) under-appreciation. The talk describes some evidence from our lab supporting these claims.

Recent years have seen a considerable surge of research on interest-based engagement, examining how and why people are engaged in activities without relying on extrinsic rewards. However, the field of inquiry has been somewhat segregated into three different research traditions which have been developed relatively independently -- research on curiosity, interest, and trait curiosity/interest. The current talk sets out an integrative perspective; the reward-learning framework of knowledge acquisition. This conceptual framework takes on the basic premise of existing reward-learning models of information seeking: that knowledge acquisition serves as an inherent reward, which reinforces people’s information-seeking behavior through a reward-learning process. However, the framework reveals how the knowledge-acquisition process is sustained and boosted over a long period of time in real-life settings, allowing us to integrate the different research traditions within reward-learning models. The framework also characterizes the knowledge-acquisition process with four distinct features that are not present in the reward-learning process with extrinsic rewards -- (1) cumulativeness, (2) selectivity, (3) vulnerability, and (4) under-appreciation. The talk describes some evidence from our lab supporting these claims.

Using a combination of in vivo imaging of neuronal circuit functional and structural dynamics, we have investigated the mechanisms by which patterned neural activity and sensory experience alter connectivity in the developing brain. We have identified, in addition to the long-hypothesized Hebbian structural plasticity mechanisms, a kind of plasticity induced by the absence of correlated firing that we dubbed “Stentian plasticity”. In the talk I will discuss the phenomenology and some mechanistic insights regarding Stentian mechanisms in brain development. Further, I will show how glia may have a key role in circuit remodeling during development. These studies have led us to an appreciation of the importance of neuron-glia interactions in early development and the ability of patterned activity to guide circuit wiring.

Microglia are the immune cells of the brain, and play increasingly appreciated roles in synapse formation, brain plasticity, and cognition. A growing appreciation that the immune system involved in diseases like schizophrenia, epilepsy, and neurodegenerative diseases has led to renewed interest in how microglia regulate synaptic connectivity. Our group previously identified the IL-1 family cytokine Interleukin-33 (IL-33) as a novel regulator of microglial activation and function. I will discuss a mechanism by which microglia regulate synaptic plasticity and long-term memories by engulfing brain extracellular matrix (ECM) proteins. These studies raise the question of how these pathways may be altered or could be modified in the context of disease.