Biology subjects

Li, B. Y.

Publications and source records attributed to Li, B. Y..

3 recordsLinked to original sources

bioRxiv2025

Synchronized path-integration recalibration but distinct landmark-control dynamics in head direction and CA1 place cells

Accurate spatial navigation relies on path integration, a process of tracking ones location by integrating self-motion cues. Path integration uses a gain factor relating self-motion signals to displacement on the cognitive map. This gain is plastic, recalibrating rapidly to match perceived displacements relative to external cues. To elucidate the mechanism of recalibration, we simultaneously recorded from place cells, which instantiate the cognitive map, and head direction (HD) cells, thought to orient the map. Persistent conflict between self-motion and visual feedback induced functionally identical recalibration of path-integration gain in the two neural populations during forward locomotion; however, during locomotor immobility accompanied by head-scanning, HD cells did not exhibit recalibration. Moreover, the two populations manifested differential field-shifting dynamics relative to landmarks during recalibration. These results uncover a tightly coordinated yet behavior-dependent recalibration process across the navigation circuit that achieves a robust yet flexible coupling of the internal sense of position and direction.

neuroscience↗

bioRxiv2022

Closed-loop control and recalibration of place cells by optic flow

Understanding the interplay between sensory input, endogenous neural dynamics, and behavioral output is key toward understanding the principles of neural computation. Hippocampal place cells are an ideal system to investigate this closed-loop interaction, as they are influenced by both self-motion (idiothetic) signals and by external sensory landmarks as an animal navigates its environment1-9. To continuously update a position signal on an internal "cognitive map", the hippocampal system integrates self-motion signals over time10,11. In the absence of stable, external landmarks, however, these spatial correlates of neuronal activity can quickly accumulate error and cause the internal representation of position or direction to drift relative to the external environment1,5. We have previously demonstrated that, in addition to their known roles in preventing and/or correcting path-integration error, external landmarks can be used as a putative teaching signal to recalibrate the gain of the path integration system6. However, it remains unclear whether idiothetic cues, such as optic flow, exert sufficient influence on the cognitive map to enable recalibration of path integration, or if instead an unambiguous allocentric frame of reference, anchored by polarizing landmark information, is essential for path integration recalibration. Here, we use principles of control theory12,13 to demonstrate systematic control of place fields by pure optic flow information in freely moving animals by using a neurally closed-loop virtual reality system that adjusts optic flow speed as a function of real-time decoding of the hippocampal spatial map. Using this "cognitive clamp", we show that we can not only bring the updating of the map under control of the optic flow cues but we can also elicit recalibration of path integration. This finding demonstrates that the brain continuously rebalances the influence of conflicting idiothetic cues to fine-tune the neural dynamics of path integration, and that this recalibration process does not require a top-down, unambiguous position signal from landmarks.

neuroscience↗

bioRxiv2018

Coordinated host-pathogen transcriptional dynamics revealed using sorted subpopulations and single, Candida albicans infected macrophages

The outcome of fungal infections depends on interactions with innate immune cells. Within a population of macrophages encountering C. albicans, there are distinct host-pathogen trajectories; however, little is known about the molecular heterogeneity that governs these fates. We developed an experimental system to separate interaction stages and single macrophage cells infected with C. albicans from uninfected cells and assessed transcriptional variability in the host and fungus. Macrophages displayed an initial up-regulation of pathways involved in phagocytosis and proinflammatory response after C. albicans exposure that declined during later time points. Phagocytosed C. albicans shifted expression programs to survive the nutrient poor phagosome and remodeled the cell wall. The transcriptomes of single infected macrophages and phagocytosed C. albicans revealed a tightly coordinated shift in gene expression co-stages and revealed expression bimodality and differential splicing that may drive infection outcome. This work establishes an approach for studying host-pathogen trajectories to resolve heterogeneity in dynamic populations.

genomics↗