The neuroscientists explain that while awake, our brain basically consists of disjointed neuronal voices chattering among themselves to allow us to work through life’s daily tasks. But while asleep, the voices of signaling neurons meld into a unified chorus of bursts, which neuroscientists call slow-wave activity. Research suggests that astrocytes, not just neurons, may help trigger this switch.
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Astrocytes are a type of so-called glial cell that blanket the brain with countless bushy tendrils and make up around 25 to 30 percent of brain cells. Each individual astrocyte is able to listen in on tens of thousands of synapses. These cells connect to each other through specialized channels, which the researchers think may allow astrocytes located across the brain to function as one unified network.
Kira Poskanzer, senior author, said, “This could give us new insights not only into sleep but into diseases in which sleep dysregulation is a symptom. Maybe some diseases are affecting astrocytes in a way we hadn’t thought about before.”
The research team monitored changes in slow-wave activity in mice brains by manipulating astrocytes with a drug that can ‘switch on’ the cells in genetically engineered animals.
Slow-wave activity can be represented similarly to vibrations from an earthquake on a seismograph. When the brain is awake, the traces are a dense scribble of short and jerky motions, but during sleep, the signal slows, lazily looping up and down to create a trace with deep valleys and high peaks.
Findings revealed that excitation of astrocytes increased slow-wave activity, and thus sleep, in the mice. In addition, the team also found that triggering astrocytes in one part of the cortex could affect neuronal behavior at a distant point.
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The research team also studied receptor molecules that allow astrocytes to respond to signals coming from neurons and other cells. They found that two of these molecules (the Gi and Gq receptors) each appeared to control a distinct aspect of sleep.
Activating Gq receptors made animals sleep longer, but not more deeply, while activation of Gi receptors put them into a much deeper slumber without affecting sleep duration.
The authors add that the findings could open new avenues for exploring sleep disorder therapies and help scientists better understand brain diseases linked to sleep disturbances, like Alzheimer’s and other dementias.
Source: Eurekalert
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