Laura Bojarskaite from Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo is visiting Aarhus and will give a guest talk at the CFIN and MIB seminar series about mice sleeping and brain activity.

11.11.2019 | Henriette Blæsild Vuust

Laura Bojarskaite, BSc, MSc
PhD Candidate in Neuroscience
GliaLab, Letten Center
Division of Physiology
Department of Molecular Medicine
Institute of Basic Medical Sciences
University of Oslo

Title: Ca²⁺ signaling in astrocytes is sleep-wake state specific and modulated sleep

Abstract:

We spend approximately one third of our lives sleeping. The purpose of sleep is one of the greatest unsolved mysteries in biology, although it is increasingly clear that sleep is important for higher-order cognitive functions and restoration. Still, the nightlife of the housekeepers of the brain – the astrocytes – is poorly characterized. There is evidence that astrocytes regulate sleep drive, promote sleep-dependent brain waste clearance and facilitate cortical oscillations that are important for learning and memory, but the signaling mechanisms that astrocytes employ to mediate these sleep-dependent functions remain elusive. Astrocytic Ca²⁺ signals are considered to orchestrate neuronal circuits by regulating the extracellular ion concentration and promoting the release of signaling substances. In addition, astrocytes not only sense local synaptic activity, but also respond with Ca²⁺ signals to neuromodulators that are involved in sleep-wake state regulation. Whereas attempts have been made to image astrocytic Ca²⁺ signals under anesthetic conditions mimicking sleep, astrocytic Ca²⁺ signaling in natural sleep has not yet been characterized. Here, we employed a novel activity-based algorithm to assess astrocytic Ca²⁺ signals in the somatosensory cortex of awake and naturally sleeping mice while monitoring neuronal Ca²⁺ activity, brain rhythms and behavior. We discovered that Ca²⁺ signaling in astrocytes exhibits distinct features across the sleep-wake cycle and is reduced in sleep compared to wakefulness. Moreover, an increase in astrocytic Ca²⁺ signaling precedes transitions from slow-wave sleep to wakefulness, with a peak upon awakening exceeding the levels during whisking and locomotion. Genetic ablation of a key astrocytic Ca²⁺ signaling pathway resulted in fragmentation of slow-wave sleep, yet increased the frequency of sleep spindles. Our findings demonstrate an essential role of astrocytic Ca²⁺ signaling in modulating sleep.

Find article at:
https://www.biorxiv.org/content/10.1101/750281v1.full

ALL ARE WELCOME