Cortical astrocytes play key roles in NREM sleep by regulating sleep depth and duration through separate GPCR pathways, and differentially control neuronal slow-wave activity in local and remote cortical circuits.

Parenchymal astrocytes are quiescent neural stem cells whose neurogenic potential can be unleashed by targeted manipulations guided by single-cell RNA sequencing data.

A new strategy of memory consolidation disruption based on astrocyte and purinergic signaling, which leads to persistent fear memory attenuation accompanied by reduced fear-related anxiety behavior.

Promoting a Warburg-like shift in astrocytic metabolism through reduced mitochondrial electron transport accommodates the energetic burden caused by brain trauma without overwhelming cellular respiration and redox to salvage dopaminergic neurons.

Brain-derived neurotrophic factor (BDNF)/TrkB.T1 signaling contributes to astrocyte morphological maturation, with implications for neuronal synaptogenesis and function and astrocyte functional maturation.

The structural morphology of astrocyte processes is constrained by functional boundaries in the mouse, rat and human cortex.

Spines with multiple excitatory contacts are potential sites for competition between thalamic and cortical axons, which is regulated by the astrocytes through the secreted synaptogenic protein hevin.

Drosophila astrocytes regulate the homeostatic response to sleep need and express the AANAT1 enzyme that limits brain accumulation of serotonin and dopamine caused by overnight sleep deprivation.

Astrocytes modulate synaptic remodeling of developing circuits in a cell type-specific manner, with long lasting deficits in synaptic plasticity.

Astrocytes regulate the pruning of excitatory synapses during early life through ATP signaling.