Perturbed astrocyte Ca2+ signaling in a diet‐based mouse model of small cerebral vessel disease

The hyperhomocysteinemia (HHcy) diet model of small cerebral vessel disease exhibits vascular inflammation, cerebral hypoperfusion, impaired neurovascular coupling, synapse dysfunction, and cognitive decline. Pathological changes in astrocyte structural features have also been noted, but functional astrocyte phenotypes have not been characterized. Here, we assessed Ca2+ signaling in individual astrocytes and astrocyte networks in barrel cortex of mice, pretreated with control or HHcy diet. Investigations were performed in fully awake mice to avoid confounding interactions between anesthetics, neural circuit activity, and vasoactive factors.