Researchers discovered that the brain’s primary inhibitory neurons, called parvalbumin neurons, play a crucial role in regulating deep sleep or rebound sleep that occurs after prolonged wakefulness.

We have all experienced at one time or another that when we are sleep deprived, such as when we pull an all-nighter, we feel a strong sense of sleepiness, and our subsequent sleep is longer and deeper than usual.

This indicates that the brain has a mechanism (sleep homeostasis) that records the history of wakefulness and compensates for the sleep needed based on that history. However, the mechanism of sleep homeostasis in the brain is not well understood.

Unraveling the Mystery of Rebound Sleep

By experimentally depriving mice of sleep, this research group showed that PV-expressing neurons in the cerebral cortex are activated when sleepiness increases and rebound sleep occurs.

Furthermore, they elucidated that the activation of calcium/calmodulin-dependent kinase II (CaMKII), a protein phosphorylation enzyme, causes rebound sleep by activating PV-expressing neurons in response to sleepiness.

This study reveals a part of the molecular and neural mechanisms of sleep homeostasis, one of the major mysteries of sleep science. These results are expected to lead to the development of methods to appropriately control sleepiness while quantitatively monitoring it.

Source-Eurekalert