Sleep deprivation typically results in longer and deeper sleep, thereby maintaining overall sleep quantity and quality through homeostatic regulation. However, the specific mechanisms by which the brain monitors and controls sleep homeostasis remain unclear.
To address this, the researchers focused on synaptic connections between neurons. They developed a novel molecular tool, SYNCit-K, which enhances synaptic strength, and EIN (excitatory-inhibitory neuronal network) model, a mathematical framework predicting the relationship between synaptic strength and brain activity. Application of SYNCit-K to the frontal cortex of mice induced sleep, while inhibition of synaptic enhancement prevented the induction of deep sleep. Enhanced synaptic strength in the prefrontal cortex returned to normal levels following subsequent sleep. These findings aligned with predictions from the EIN model, elucidating how increased synaptic connections in the brain induce sleep.
Understanding the role of synaptic strength in sleep homeostasis offers potential for developing new therapeutic approaches to improve sleep quantity and quality. Moreover, expanding the application of SYNCit-K and the EIN model could advance the understanding of brain functions and the computational theories underlying sleep.
Title of original paper: Prefrontal synaptic regulation of homeostatic sleep pressure revealed via synaptic chemogenetics
Journal:Science
