7 No. 4
of a Lullaby
In Emory's growing sleep
research program, scholars encounter mystery and paradox
breath and life
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
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
Power of Sleep
Exploring disorder and disturbance
P. Parker, Edith F. Honeycutt Professor of Nursing
A Few Drinks Between Friends?
the ancient drinking party with students
Bing, Associate Professor of Classics
and Transformative Knowledge
Practicing what we profess
D. Scheib, Associate Professor of Pastoral Care and Pastoral Theology
Exchange: Can you explain how circadian rhythms operate?
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
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.
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