Sleep is a universal behaviour across the animal kingdom and humans spend on average one-third of their lives asleep. Surprisingly, the full picture of how sleep is regulated and why we need sleep is still yet to be completed. In mammals, sleep consists of two phases: rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep. Both REM and NREM sleep are chronologically and homeostatically regulated by several brain regions. Previous studies have established the association between sleep disturbances and almost all the neurological disorders, including autism, Alzheimer’s disease and Parkinson’s disease. In addition, sleep has also been compared to sedation, a state sharing significant behavioural similarities with sleep, such as reduced movements, enhanced slow-wave activity and lowered body temperature. Whether sedatives work through a common mechanism of hijacking the sleep-regulating circuits still remains elusive.
This project aimed to identify novel neuronal circuits controlling sleep and sedation. Discoveries of this project would significantly advance our understanding of the fundamental mechanisms of sleep/sedation and provide novel insights into how sleep is linked with various neurological disorders. It would also offer potential therapeutic strategies and contribute to designing more efficient and safer medications.
The main scientific goal was broken down into the following three objectives:
- To evaluate alterations of excitatory/inhibitory input onto defined LPO neurons during prolonged wakefulness and sedation.
- To identify the origin of inputs onto the defined LPO neurons
- To determine the effects of altered connectivity involving active LPO neurons on sleep and sedation status in vivo.
