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

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.

Astrocyte microdomain calcium transients are mediated by TrpML, stimulated by ROS and tyramine, and mediate astrocyte–tracheal interactions in CNS gas exchange.

A single astrocyte can decode neuronal activity and, consequently, release distinct gliotransmitters that differentially regulate neurotransmission at single hippocampal synapses.

Increased spontaneous calcium activity in Rett syndrome astrocytes is a key cell-autonomous phenotype that affects synaptic function and network activity.

Astrocytes impact neuronal signaling in brain dependent on status of the transcriptional repressor, Methyl CpG Binding Protein 2.

Astrocytes modulate neuronal networks during hypercapnia, introducing a novel gliotransmitter pathway where prostaglandin E2 regulates breathing.

Astrocytes decode temporal interneuron activity and transform inhibitory into excitatory signals that impact excitatory synaptic strength and neuronal circuit function.