Anatomy of a Lullaby

I think there are valuable things we can learn about how plastic or mutable the circadian system is by looking at people who travel abroad and contend with jet lag, or people from different cultures.

—Hillary Rodman, Associate Professor of Psychology


 

Vol. 7 No. 4
February/March 2005

Anatomy of a Lullaby
In Emory's growing sleep research program, scholars encounter mystery and paradox

Stealing breath and life
Sleep Apnea

We do have some very good people [in sleep research], and we’re gaining a critical mass to do this kind of work.
Donald L. Bliwise, Professor of Neurology, Program Director, Sleep, Aging and Chronobiology


I think there are valuable things we can learn about how plastic or mutable the circadian system is by looking at people who travel abroad and contend with jet lag, or people from different cultures.
Hillary Rodman, Associate Professor of Psychology


The Power of Sleep
Exploring disorder and disturbance
Kathy P. Parker, Edith F. Honeycutt Professor of Nursing

What’s A Few Drinks Between Friends?
Exploring the ancient drinking party with students
Peter Bing, Associate Professor of Classics

Transforming
and Transformative Knowledge

Practicing what we profess
Karen D. Scheib, Associate Professor of Pastoral Care and Pastoral Theology

Further reading

Endnotes

Return to Contents

Academic Exchange: Can you explain how circadian rhythms operate?

Hillary Rodman: There is a tiny subdivision of the brain called the suprachiasmatic nucleus (SCN) that sits above where the optic nerves cross. It’s equipped with cells that function as tiny pacemakers that are literally turned on and off by different neurochemicals, and they’re indirectly controlled by other influences throughout the brain that are involved in arousal, attention, and memory. These pacemaker cells receive input from cells in the retina; they synchronize their activity with the outside world by measuring light levels in the environment, and they’re able to orchestrate shifts in wakefulness, temperature, hormone production, digestion, and a whole variety of physiological and behavioral functions.

This shred of brain is basically the day-night pacemaker, but it can also be affected by what’s going on in the environment. So if you know you normally get tired or go to bed at midnight, but you’re really agitated or interested in something that’s going on, you can sometimes override these intrinsic signals. Why that is and why different people are differentially susceptible to overriding those signals, we’re not sure. I’m interested in looking in different brain regions that turn on and off at different times of the day and provide input to the scn that potentially tells it to wait a bit and reset its circadian patterning.

AE: What part does light play in circadian rhythms?

HR: It turns out there are special retinal ganglion cells in the retina that were just discovered a couple of years ago. These special cells send information directly to portions of the scn to reset its intrinsic rhythm. The finding contradicts the traditional story of how the retina works. The traditional story I used to tell students is that light enters the eye, hits the rod and cone cells, then there are a couple of intermediate stages before the information finally hits the scn. But it turns out that there are retinal ganglion cells that are light sensitive and that talk directly to the brain. You don’t even need the rods and cones to set the circadian clock. There’s this really amazing specialized system in the retina of several kinds of rodents, and presumably primates also, that provides a direct pathway from the retina to the tiny circadian pacemaker at the bottom of the brain.

AE: Do circadian rhythms behave differently as the length of daylight changes through the seasons?

HR: That gets back to what is the normal variation in sleep behavior and what is pathology. I see students expressing a lot of guilt about individual variations in their sleep behavior. I think I’ve been more focused on our own culture, and on our microcosm of our academic world. But I think there are valuable things we can learn about how plastic or mutable the circadian system is by looking at people who travel abroad and contend with jet lag, or people from different cultures. All of a sudden you learn that things are very different under different environmental conditions, and that makes you wonder if the eight-hour rule is just a myth. Human evolution hasn’t been going on for very long. If people in other cultures can adapt to broken sleep and spend a couple hours awake in the middle of night, that indicates that there’s something in our brains that permits that to be a successful strategy.

AE: How effective are stimulants such as caffeine for alleviating sleep deprivation?

HR: One of interesting things we know now about sleep deprivation is that there seem to be chemicals that build up as the sleep debt builds. This idea of a sleep chemical—a somnogen—that you have to discharge to remain awake, has actually been around for centuries. One chemical that does build up is adenosine, which is a by-product of energy production in the body. It tends to build up particularly in regions of the brain associated with sleep. Caffeine keeps adenosine molecules from reaching their receptor sites. When you drink coffee, you’re taking an intrinsic sleep chemical and kicking it out of its chemical place in the nervous system and postponing its effects. Postponing is the key word. As soon as you stop drinking coffee, there’s still all this adenosine left over. In the short term you feel the effects of the caffeine, but you have to keep drinking it to maintain that effect. But if you haven’t gotten enough sleep, drinking coffee ultimately doesn’t help.