Kamal Ghorui
We have all been there: staying over at a relative’s house or checking into a new hotel, only to spend the night tossing and turning. Despite the plush pillows, soft lighting, and perfect room temperature, eyes are wide open at 3 am. The body is exhausted, the bed is more than comfy, and yet, sleep refuses to show up. For decades, scientists knew that the ‘first night effect’ was real, but the reason why the brain sabotages rest in new places remained unclear.Scientists at the Nagoya University wanted to understand why this happens. And guess, what? They found the reason behind this first night effect. The findings of the study is published in Proceedings of the National Academy of Sciences.
Why sleep gets affected in new environments
You might have noticed that, on the first day of checking into a hotel, you toss and turn all night. But, surprisingly, sleep improves the following night. What’s the reason behind it? To understand this, the researchers experimented on mice. They identified a group of neurons that become active when an animal enters a new environment. These neurons release a molecule called neurotensin that maintains wakefulness. The effect protects them from potential dangers in unknown surroundings.
The first night effect
When you check into a new hotel room, your brain doesn’t see a cozy bed, it senses potential danger. The new findings may explain the ‘first night effect’ seen in humans. The brain becomes more vigilant on the first night in a new place. It acts as a night guard. It keeps one eye open until it confirms the environment is safe. This response evolved to enhance survival. Though intensive research has been done on this sleep disturbance for decades, the brain mechanism behind it had remained unclear.“The extended amygdala is a brain region that processes emotions and stress in mammals. Within this region, specific neurons called IPACL (Interstitial Part of the Anterior Central Amygdala) CRF neurons produce neurotensin and activate when sensing a new environment. Neurotensin then affects the substantia nigra, a brain area that controls movement and alertness,” Daisuke Ono, senior author and lecturer at Nagoya University’s Research Institute of Environmental Medicine, said in a release.The researchers studied mice in new cages and recorded their brain activity. They noticed that IPACL CRF neurons became highly active in their new environments. To confirm the cause, the researchers artificially suppressed these neurons, and they found the mice falling asleep quickly, despite being in new environments. When these neurons were activated, the mice stayed awake longer. The team showed that IPACL CRF neurons use neurotensin to communicate with the substantia nigra.The researchers think that similar circuits likely operate in humans, as the extended amygdala and substantia nigra exist in all mammals. These new findings could help develop new treatments for insomnia and anxiety disorders. Many people with PTSD or chronic stress experience excessive nighttime alertness. Drugs that target this neurotensin pathway could help them sleep.
