Nagoya – An international research team from Nagoya University has discovered the neural mechanism behind why humans (and mice) often sleep poorly in new environments. Specific neurons in the extended amygdala (IPACL CRF neurons) become active as soon as an animal enters an unfamiliar environment. These neurons release neurotensin, which maintains wakefulness – a protective response that minimizes potential dangers in unknown locations. The study was published in the Proceedings of the National Academy of Sciences.
The phenomenon is known as the "First Night Effect": On the first night in a hotel or a strange bed, the brain remains vigilant, almost like a night watchman, until safety is confirmed. This vigilance is evolutionarily sensible but has not been understood at the cellular level until now.
The researchers studied mice in new cages and recorded their brain activity. IPACL CRF neurons fired strongly in unfamiliar environments. When this activity was artificially suppressed, the mice quickly fell asleep – even in new cages. When artificially activated, they remained awake significantly longer. Neurotensin acts on the substantia nigra, a region that regulates motor control and wakefulness.
The findings explain the "First Night Effect" in humans: The extended amygdala and the substantia nigra exist in all mammals, so a similar mechanism is likely active in us as well.
The discovery opens up new therapeutic approaches for sleep disorders and anxiety disorders. Many people with PTSD or chronic stress suffer from excessive nocturnal vigilance. Medications that specifically modulate this neurotensin pathway could help improve sleep without completely shutting down alertness.
