Astrocyte GR Signaling Reopens 3-4 Day Visual Plasticity in Adult Mice
Updated
Updated · Nature.com · May 20
Astrocyte GR Signaling Reopens 3-4 Day Visual Plasticity in Adult Mice
1 articles · Updated · Nature.com · May 20
Adult mice regained ocular dominance plasticity after 3-4 days of monocular deprivation when glucocorticoid receptor signaling was deleted specifically in visual-cortex astrocytes, while normal visual responses stayed unchanged without deprivation.
6,274 light-induced GR binding sites in astrocytes linked eye opening to a corticosterone rise around postnatal day 14, triggering gene programs that mature astrocytes and help close the visual system’s critical period.
GR loss reduced astrocyte territory and process infiltration, weakened perineuronal nets on parvalbumin interneurons, and shifted inhibitory wiring by lowering PV synapses while increasing CCK synapses onto layer-5 neurons.
Single-cell and chromatin analyses across 70,907 mouse V1 cells also showed astrocyte GR suppression reactivated neuronal axonal-sprouting genes, suggesting astrocytes impose structural brakes on cortical plasticity.
Human developmental datasets showed GR motif accessibility rising in astrocytes from late gestation into adolescence, indicating parts of this maturation pathway are conserved and may link early-life stress to neuropsychiatric risk.
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Astrocytes as Master Regulators: New Mechanisms and Therapeutic Frontiers in Adult Brain Plasticity
Overview
For many years, neurons were seen as the main drivers of brain plasticity, while astrocytes were thought to play only a supporting role. However, new research has sparked a major shift in this view. Scientists now recognize that astrocytes are active regulators of brain function, especially in adults. Astrocytes not only secrete neuroactive molecules and help form and mature synapses, but they also respond to neurotransmitters by releasing their own signals, called gliotransmitters, which influence how neurons communicate. Recent discoveries show that astrocytes are crucial for both promoting plasticity during development and shutting down critical periods, helping to maintain stability in the adult brain.