AI Article Synopsis
- Scientists studied how sleep is regulated in male mice, especially after staying awake for a long time.
- They found that a special protein called CaMKII helps control certain brain cells (called PV neurons) that are important for sleep.
- When these PV neurons become more active, it leads to more rebound sleep, which happens after being awake for too long.
Article Abstract
The homeostatic regulation of sleep is characterized by rebound sleep after prolonged wakefulness, but the molecular and cellular mechanisms underlying this regulation are still unknown. In this study, we show that Ca/calmodulin-dependent protein kinase II (CaMKII)-dependent activity control of parvalbumin (PV)-expressing cortical neurons is involved in homeostatic regulation of sleep in male mice. Prolonged wakefulness enhances cortical PV-neuron activity. Chemogenetic suppression or activation of cortical PV neurons inhibits or induces rebound sleep, implying that rebound sleep is dependent on increased activity of cortical PV neurons. Furthermore, we discovered that CaMKII kinase activity boosts the activity of cortical PV neurons, and that kinase activity is important for homeostatic sleep rebound. Here, we propose that CaMKII-dependent PV-neuron activity represents negative feedback inhibition of cortical neural excitability, which serves as the distributive cortical circuits for sleep homeostatic regulation.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11258272 | PMC |
| http://dx.doi.org/10.1038/s41467-024-50168-5 | DOI Listing |
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