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

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

Extracellular vesicles are proposed as novel, non-cell-autonomous mediators of neuronal atrophy in Parkinson's disease.

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

Noradrenaline-mediated astrocytic Ca²⁺ signaling in behavior is reduced in awake-behaving tg-ArcSwe Alzheimer's disease transgenic mice.

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

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

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

In astrocytes, there exists an intrinsic spatial threshold of subcellular calcium levels that triggers an astrocyte calcium surge throughout the cell, demonstrating cellular astrocyte calcium integration of time and space.

Analysis of a mouse model of megalencephalic leukoencephalopathy with subcortical cysts (MLC) shows that the astrocyte-specific membrane protein MLC1 sustains the postnatal development of perivascular astrocytic processes and that MLC is a developmental disorder of the gliovascular unit.