The findings of Dr. Constantin Von Economo, who autopsied victims of sleeping sickness in the 1920s, were prescient. Researchers who went on to study the brains of rats and other lab animals confirmed his theory of a “sleep regulating center” in the brain. While damage to the rear of the hypothalamus sent the animals into a coma, damage to the front gave them a terrific case of insomnia.
Clearly some very important processes took place in the front and rear areas of the hypothalamus, a grape-sized structure deep in the brain.
Sleep Switch at the Front
The front part of the hypothalamus is now known to contain a small cluster of neurons called the VLPO, and they produce GABA and galanin, neurochemicals highly conducive to sleep.
These neurons are mostly off-duty during the daytime. But at night they come alive. When sleep pressure builds up high enough, the VLPO neurons start firing away like mad. Current theory holds that they’re powerful enough to shut the rest of the brain down, in essence functioning like a “sleep switch.”
Alerting Force in the Rear
At the rear of the hypothalamus is an important set of neurons that have the opposite effect: when they’re firing, they help keep you awake. They produce a substance called orexin, and they function “like a ‘finger’ on the (sleep) switch that might prevent unwanted transitions to sleep,” sleep scientist Clifford Saper has said.
The sleep-friendly neurons in the VLPO work to “tranquilize” the orexin neurons at night. But people with a substantial loss of orexin neurons experience narcolepsy. Narcoleptics have irresistible sleep attacks during the day and they also have trouble staying asleep at night. The trusty “finger” on the sleep switch, which helps to maintain a stable waking state, just isn’t there.
How This Relates to Insomnia
A deterioration of orexin neurons may also be a factor in the insomnia of older adults, Saper has hypothesized. Like narcoleptics, older adults tend to nap a lot during the daytime and have frequent wake-ups at night.
A causal factor of insomnia in younger adults, on the other hand, could be a reduced number of GABA neurons in the brain, or an overabundance of orexin neurons. Either condition could interfere with the sleep switch enabling quick, easy transitions to sleep.
These theories aren’t of practical value yet. But stay tuned. The FDA is reviewing a completely new insomnia medication – the first ever “orexin receptor antagonist” – right now.