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Striatal cholinergic interneurons and astrocytes lose cilia and show dysregulation of Hedgehog signaling in mice with a Parkinson's disease-associated, G2019S LRRK2 mutation or upon loss of PPM1H phosphatase specific for LRRK2-phosphorylated Rab GTPases.

Exposing rats to acute stress increased the generation of new neurons in a subregion of the hippocampus, and improved the animals' performance in a memory task two weeks later.

Amygdala astrocytes play a critical role in mediating the effects of stress during infancy on neuronal excitability, synaptic plasticity, and memory.

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.

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

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

Electrophysiology experiments with genetic and pharmacological manipulations identify a role for astrocyte GluN2C NMDA receptors in maintaining the broad range of presynaptic strengths, which is suggested by numerical simulations to enhance the expression of synaptic plasticity.

Cell biology and animal model analysis in mice shows that molecules involved in glycolytic metabolism could potentially serve as therapeutic targets for the treatment of neurological diseases.

Two different forms of brain plasticity require astrocytes and show different action mechanisms at enthorrinal cortex hippocampal synapses.

Serum response factor (SRF) deficient reactive astrocytes are neuroprotective in the mammalian brain.