In the first study, the research group of Jan Deussing explored a genetic variation in the P2X7 receptor that previously has been associated with depression and anxiety. They found that when they engineered mice to have one copy of this gene variant (heterozygous) the mice had sleep disturbances and impaired receptor function in addition to a higher vulnerability to stress. They then looked at the effect of this variant in humans. Similarly to the mice, they found that heterozygous individuals had changes in their sleep patterns.
Deussing concludes: “This is an exciting finding as it suggests that altered P2X7R function in heterozygote individuals disturbs sleep, which might explain their increased risk for developing mood disorders”.
In the second study, Mayumi Kimura and colleagues investigated how prepubertal obesity can affect sleep in later life. They wanted to see what happens to sleep patterns in adult mice when they are given an obesity inducing diet around the time of puberty. They found that this temporary change in diet was enough to cause profound alterations in sleep that persisted for life.
The scientists went on to identify the mechanism that could account for the persistent alterations in sleep. They found that the mice who were given the high-fat diet had blunted serotonergic signaling in the lateral hypothalamus. Moreover, they were able to reverse this blunted signaling by giving the mice a peptide that is normally released by the gut upon satiety. This peptide was also able to restore the sleep pattern back to normal.
“These studies are an important step forward,” concludes Alon Chen, Director of the Max Planck Institute of Psychiatry, “finally we’re getting some answers for a more mechanistic understanding of the role sleep plays in psychiatric illness”.