Symposium
Session Room: Carron
Session Room: Carron
Monday, June 29, 10:50 AM – 12:05 PM
Symposium 24:
Neuron-Astrocyte Interaction in Striatopallidal Circuits for Decision-Making, Eating Behavior, and Behavioral Flexibility
Neuron-Astrocyte Interaction in Striatopallidal Circuits for Decision-Making, Eating Behavior, and Behavioral Flexibility
This symposium brings together recent advances in the understanding of cortico-basal ganglia circuitry underlying decision-making, reward processing, and behavioral flexibility. It focuses on the integration of neuronal and astrocytic mechanisms across striatal and pallidal networks.
Dr. de Kerchove d’Exaerde will present a framework describing how decision-making can be modeled through reinforcement learning principles, emphasizing how sensitivity to risk and reward is differentially modulated across learning profiles, striatal subregions, and cell types (Bonnavion et al., 2024, Rodriguez et al., 2025, Varin et al., 2023). In his recent study, decision-making in mice was characterized by three stable strategies—Optimizers, Risk-averse, and Explorers—each governed by distinct neural dynamics within the striatum. Using a mouse gambling task combined with computational modeling, his team demonstrated that these behavioral strategies reflect varying sensitivities to reward magnitude, risk, and punishment. Chemogenetic manipulations revealed that dorsomedial striatum (DMS) neurons play a pivotal role in shaping decision-making: direct pathway neurons (dSPNs) reduce risk aversion by increasing the perceived value of risky choices, whereas indirect pathway neurons (iSPNs) heighten sensitivity to large rewards. These findings suggest that decision-related disorders such as gambling and addiction may emerge from evolutionary trade-offs in decision-making profiles.
Dr. Montalban will then explore the interface between reward processing and metabolic regulation of eating behavior, revealing how striatal neurons and astrocytes jointly regulate peripheral metabolic states (Montalban et al., 2025, Montalban et al., 2024, Montalban et al., 2023). Her work demonstrates that loss of control over palatable food consumption is linked to gene expression changes specifically within dopamine D2 receptor–expressing neurons of the striatum. Manipulating the activity of striatal astrocytes alters both metabolism and cognitive flexibility during exposure to an obesogenic diet. Furthermore, selective modulation of Ankk1 expression in D2 neurons reproduces the metabolic and reward phenotypes seen in humans carrying the Taq1A polymorphism in the Ankk1 gene. Collectively, these findings position the striatum as a central hub for body–brain interactions, integrating metabolic and reward pathways relevant to disorders such as obesity and compulsive eating.
Finally, Dr. Choi will present recent discoveries on how pallidal neurons and astrocytes, as downstream targets of striatal output, contribute to reversal learning and behavioral flexibility (Baker et al., 2023, Kang et al., 2023, Kang et al., 2025). His work identifies two major GPe cell types—prototypic neurons projecting to the subthalamic nucleus (Proto: GPe→STN) and astrocytes—as key mediators of adaptive behavior. Reversal learning tasks revealed that Proto: GPe→STN neurons dynamically encode contextual information that correlates with behavioral optimality, whereas GPe astrocytes show gradual contextual encoding independent of task performance. Deletion of Proto: GPe→STN neurons selectively disrupted adaptive responses to changing contingencies without affecting initial reward acquisition. These neurons integrate inhibitory striatal and excitatory subthalamic inputs, with astrocytic modulation likely shaping non-canonical information flow for flexible reward-seeking behavior.
Together, these presentations will highlight emerging concepts on neuronal and astrocytic contributions to adaptive decision-making, reward valuation, and metabolic regulation, offering a multi-dimensional view of striatal and pallidal circuitry and their relevance to neuropsychiatric disorders.
Dr. de Kerchove d’Exaerde will present a framework describing how decision-making can be modeled through reinforcement learning principles, emphasizing how sensitivity to risk and reward is differentially modulated across learning profiles, striatal subregions, and cell types (Bonnavion et al., 2024, Rodriguez et al., 2025, Varin et al., 2023). In his recent study, decision-making in mice was characterized by three stable strategies—Optimizers, Risk-averse, and Explorers—each governed by distinct neural dynamics within the striatum. Using a mouse gambling task combined with computational modeling, his team demonstrated that these behavioral strategies reflect varying sensitivities to reward magnitude, risk, and punishment. Chemogenetic manipulations revealed that dorsomedial striatum (DMS) neurons play a pivotal role in shaping decision-making: direct pathway neurons (dSPNs) reduce risk aversion by increasing the perceived value of risky choices, whereas indirect pathway neurons (iSPNs) heighten sensitivity to large rewards. These findings suggest that decision-related disorders such as gambling and addiction may emerge from evolutionary trade-offs in decision-making profiles.
Dr. Montalban will then explore the interface between reward processing and metabolic regulation of eating behavior, revealing how striatal neurons and astrocytes jointly regulate peripheral metabolic states (Montalban et al., 2025, Montalban et al., 2024, Montalban et al., 2023). Her work demonstrates that loss of control over palatable food consumption is linked to gene expression changes specifically within dopamine D2 receptor–expressing neurons of the striatum. Manipulating the activity of striatal astrocytes alters both metabolism and cognitive flexibility during exposure to an obesogenic diet. Furthermore, selective modulation of Ankk1 expression in D2 neurons reproduces the metabolic and reward phenotypes seen in humans carrying the Taq1A polymorphism in the Ankk1 gene. Collectively, these findings position the striatum as a central hub for body–brain interactions, integrating metabolic and reward pathways relevant to disorders such as obesity and compulsive eating.
Finally, Dr. Choi will present recent discoveries on how pallidal neurons and astrocytes, as downstream targets of striatal output, contribute to reversal learning and behavioral flexibility (Baker et al., 2023, Kang et al., 2023, Kang et al., 2025). His work identifies two major GPe cell types—prototypic neurons projecting to the subthalamic nucleus (Proto: GPe→STN) and astrocytes—as key mediators of adaptive behavior. Reversal learning tasks revealed that Proto: GPe→STN neurons dynamically encode contextual information that correlates with behavioral optimality, whereas GPe astrocytes show gradual contextual encoding independent of task performance. Deletion of Proto: GPe→STN neurons selectively disrupted adaptive responses to changing contingencies without affecting initial reward acquisition. These neurons integrate inhibitory striatal and excitatory subthalamic inputs, with astrocytic modulation likely shaping non-canonical information flow for flexible reward-seeking behavior.
Together, these presentations will highlight emerging concepts on neuronal and astrocytic contributions to adaptive decision-making, reward valuation, and metabolic regulation, offering a multi-dimensional view of striatal and pallidal circuitry and their relevance to neuropsychiatric disorders.