Abstract
How the brain controls the need and acquisition of recovery sleep after prolonged wakefulness is an important issue in sleep research. The monoamines serotonin and dopamine are key regulators of sleep in mammals and in Drosophila. We found that the enzyme arylalkylamine N-acetyltransferase 1 (AANAT1) is expressed by Drosophila astrocytes and specific subsets of neurons in the adult brain. AANAT1 acetylates monoamines and inactivates them, and we found that AANAT1 limited the accumulation of serotonin and dopamine in the brain upon sleep deprivation (SD). Loss of AANAT1 from astrocytes, but not from neurons, caused flies to increase their daytime recovery sleep following overnight SD. Together, these findings demonstrate a crucial role for AANAT1 and astrocytes in the regulation of monoamine bioavailability and homeostatic sleep.
Highlights
Characteristic features of sleep are conserved among species (Pimentel et al, 2016), and from humans to insects sleep is influenced by neural circuits involving monoamines such as serotonin and dopamine (Nall and Sehgal, 2014)
With cell type selective arylalkylamine N-acetyltransferase 1 (AANAT1) knockdown, we find that AANAT1 functions in astrocytes, but not neurons, to limit the amount of recovery sleep that flies take in response to sleep deprivation (SD)
AANAT1 immunoreactivity was observed in the cytoplasm of many cells (Figure 1A) but was absent in age-matched ventral nerve cords of embryos that were homozygous for a deletion of the entire AANAT1 gene (Figure 1B)
Summary
Characteristic features of sleep are conserved among species (Pimentel et al, 2016), and from humans to insects sleep is influenced by neural circuits involving monoamines such as serotonin and dopamine (Nall and Sehgal, 2014). Most research has focused on the role of different brain circuits on sleep, but it has been shown that a certain type of brain cell, known as astrocyte, may be important for sleep regulation It has been unclear if astrocytes could be involved in regulating the need for recovery sleep after a sleep-deprived night – known as rebound sleep. In mutant flies that lacked AANAT1, both dopamine and serotonin levels increased in the brain after sleep deprivation. In sleep deprived AANAT1 mutant flies, heightened recovery sleep is accompanied by increased serotonin and dopamine levels in the brain. With cell type selective AANAT1 knockdown, we find that AANAT1 functions in astrocytes, but not neurons, to limit the amount of recovery sleep that flies take in response to sleep deprivation (SD) These findings identify a critical role for astrocytes in the regulation of monoamine bioavailability and calibration of the response to sleep need
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