A lot of people question why they cannot sleep, but for neuroscientists, the more intriguing question may be why we ever wake up. "Naturally, we would always be asleep," says Jerome Siegel, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA. Siegel and other researchers have located the "stay awake" centers in the brain that drag us out of perpetual somnolence. These centers are located in the hypothalamus and the brain stem. A complex cocktail of neurotransmitters regulates them. The neurotransmitters include acetylcholine, norepinephrine, serotonin, and histamine.
But some scientists, including Siegel, think another neurotransmitter hypocretin (also called orexin) is the main chemical that pushes the "awake button" in the hypothalamus. "... [O]rexin floods the brain, waking us up," Siegel says. Brain cells that produce hypocretin are normally active during waking and inactive during sleep. During the waking hours, levels of hypocretin rise, increasing "sleep pressure," or the need to sleep.
But as any restless sleeper can attest, a number of environmental factors—including temperature, noise, and bright light—can interfere with sleep no matter how great the need to catch some much-craved ZZZs. Bright light can be a major sleep-robber. It arouses us. It can keep us awake. For neuroscientists, this fact poses an essential question: How does bright light affect sleep, wakefulness, and their root cause: hypocretin levels in the brain's sleep centers?
Now researchers at UCLA have identified the group of neurons that mediates whether light arouses us. Siegel and colleagues report in the October 26 online edition of the Journal of Neuroscience that the cells necessary for a light-induced arousal response are located in the hypothalamus, and that those cells release hypocretin.
In reaching that conclusion, the researchers examined the behavioral capabilities of mice that had their hypocretin genetically "knocked-out" (KO mice) and compared them with the activities of normal, wild-type mice (WT) that still had their hypocretin neurons. The researchers tested the two groups while the animals performed a variety of tasks during both light and dark phases. The study revealed that the animals that didn't have hypocretin were unable to stay awake in the light, while those that had it showed intense activation of particular hypothalamic cells in the light but not while they were awake in the dark.
"The findings suggest that administering hypocretin and boosting the function of hypocretin cells will increase the light-induced arousal response," Siegel said in a recent press release. "Conversely, blocking their function by administering hypocretin receptor blockers will reduce this response and thereby induce sleep." These findings point the way toward new treatments for sleep disorders and, perhaps, for seasonal affective disorder, the form of depression most affected by light levels.
For More Information:
Faith Brynie. Brain Sense.
T. Deboer, S. Overeem, N. A. H. Visser, et al. "Convergence of Circadian and Sleep Regulatory Mechanisms on Hypocretin-1," Neuroscience (July 2004), pp. 727-732.
Ronald McGregor, Ming-Fung Wu, Grace Barber, Lalini Ramanathan, and Jerome M. Siegel. "Highly Specific Role of Hypocretin (Orexin) Neurons: Differential Activation as a Function of Diurnal Phase, Operant Reinforcement versus Operant Avoidance and Light Level," Journal of Neuroscience, 26 October 2011, 31(43): 15455-15467.