Astrocytes respond proportionally to arousal changes via pupil dilation. Astrocyte Ca2+ correlates better with pupil diameter than running speed. Astrocytes sense relative changes in arousal, not absolute levels. NE increases precede astrocyte Ca2+ events. Large phasic NE drives prolonged astrocyte Ca2+ increases. Astrocyte Ca2+ peaks coincide with reductions in arousal-driven neuronal activity. Astrocytes link to bi-hemispheric cortical state transitions from desynchrony to synchrony. Adra1a receptor stimulation paradoxically boosts cortical synchrony. Astrocyte-specific Adra1a deletion enhances neuronal activity and impairs arousal-related synchrony. Astrocyte Ca2+ precedes increases in low-frequency LFP power. Neuronal Ca2+ correlates with absolute LFP power while astrocyte Ca2+ ties to LFP power changes. Prazosin blocks astrocyte-LFP synchrony link. Adra1a agonist A61603 elevates astrocyte Ca2+ and inhibits neuronal activity. A61603 shifts neuronal power to slower frequencies. Astrocytes act as feedback sensors counteracting arousal desynchrony. Local neuronal silencing does not block astrocyte arousal responses. Pupil diameter predicts astrocyte Ca2+ better than local neuronal activity.