The remarkable ability of the motor system to adapt to novel environments has traditionally been investigated using kinematically non-redundant tasks, such as planar reaching movements. This limitation prevents the study of how the motor system achieves adaptation by altering the movement patterns of our redundant body. To address this issue, we developed a redundant motor task in which participants reached for targets with the tip of a virtual stick held with both hands. Despite the redundancy of the task, participants consistently employed a stereotypical strategy of flexibly changing the tilt angle of the stick depending on the direction of tip movement. Thus, this baseline relationship between tip-movement direction and stick-tilt angle constrained both the physical and visual movement patterns of the redundant system. Our task allowed us to systematically investigate how the motor system implicitly changed both the tip-movement direction and the stick-tilt angle in response to imposed visual perturbations. Both types of perturbations, whether directly affecting the task (tip-movement direction) or not (stick-tilt angle around the tip), drove adaptation, and the patterns of implicit adaptation were guided by the baseline relationship. Consequently, tip-movement adaptation was associated with changes in stick-tilt angle, and intriguingly, even seemingly ignorable stick-tilt perturbations significantly influenced tip-movement adaptation, leading to tip-movement direction errors. These findings provide a new understanding that the baseline relationship plays a crucial role not only in how the motor system controls movement of the redundant system, but also in how it implicitly adapts to modify movement patterns.

The circadian clock, an internal time-keeping system orchestrates 24 hr rhythms in physiology and behavior by regulating rhythmic transcription in cells. Astrocytes, the most abundant glial cells, play crucial roles in CNS functions, but the impact of the circadian clock on astrocyte functions remains largely unexplored. In this study, we identified 412 circadian rhythmic transcripts in cultured mouse cortical astrocytes through RNA sequencing. Gene Ontology analysis indicated that genes involved in Ca²⁺ homeostasis are under circadian control. Notably, Herpud1 (Herp) exhibited robust circadian rhythmicity at both mRNA and protein levels, a rhythm disrupted in astrocytes lacking the circadian transcription factor, BMAL1. HERP regulated endoplasmic reticulum (ER) Ca²⁺ release by modulating the degradation of inositol 1,4,5-trisphosphate receptors (ITPRs). ATP-stimulated ER Ca²⁺ release varied with the circadian phase, being more pronounced at subjective night phase, likely due to the rhythmic expression of ITPR2. Correspondingly, ATP-stimulated cytosolic Ca²⁺ increases were heightened at the subjective night phase. This rhythmic ER Ca²⁺ response led to circadian phase-dependent variations in the phosphorylation of Connexin 43 (Ser368) and gap junctional communication. Given the role of gap junction channel (GJC) in propagating Ca²⁺ signals, we suggest that this circadian regulation of ER Ca²⁺ responses could affect astrocytic modulation of synaptic activity according to the time of day. Overall, our study enhances the understanding of how the circadian clock influences astrocyte function in the CNS, shedding light on their potential role in daily variations of brain activity and health.