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MONDAY, APRIL 19, 2004
Contact: Donna Krupa
703.967.2751 (cell)
703.527.7357 (office)
djkrupa1@aol.com
APS Newsroom: April 17-21, 2004
Washington, DC Convention Center
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Telephone: 202.249.4009
New Research Explores “Early Bird” And “Night Owl” Sleep
Patterns
An animal study finds a link in
genetics that determines our sleep patterns
Washington, DC -- Are you annoyed by cheerful
“morning people?” Do you ever wonder how “night owls” can keep going? Most
of us ask these questions because we are in between these two extremes, and
take a while to get going early in the morning and tire long before
midnight. This entire spectrum reflects the broad, normal variation in
sleep patterns in humans that is rooted in the very genetic foundations of
how our body works. Because these variations occur within our population
and differ with age, the presumption exists that the differences in sleep
patterns are controlled by complex mechanisms with contributions from
multiple genes and influenced by environmental factors.
Linking our genetic make-up and sleep related disorders
require data that compare genetic differences that might explain the basis
of sleep disorders. Knowing what causes these disorders is important --
getting a good night sleep is now a challenge for some 50 to 70 millions
American of all ages. A 2002 National Sleep Foundation annual survey
reported that nearly 40 percent of adults 30 to 64 years old, and 44 percent
of those age 18 to 29, reported that daytime sleepiness is so severe that it
interferes with work and social functioning at least a few days each month.
Excessive daytime sleepiness has been blamed on interference in cognitive
functioning, motor vehicle crashes (especially at night), poor job
performance and reduced productivity. While researchers have learned much
about the basic mechanism underlying the control of sleep and its
importance on our daily function and health, they have only just begun to
examine the complex genetic and environmental interactions that shape sleep
and health.
A New Study
An important step in this research is a new study that
involved three different strains of inbred laboratory rats and measurements
of their movement and continuous sleep in controlled environmental chambers
for three days and nights. The study examined 24-hour variations in the
animals’ slow wave sleep, activity and changes from rest to activity. The
comparisons between
the three strains have led the researchers to conclude
that there were significant variations in these measures, strongly
suggesting that the findings were due to genetic differences.
The authors of “Circadian Slow Wave Sleep and Movement
Behavior are under Genetic Control in Inbred Strains of Rat,” are Thom R
Feroah, Todd Sleeper, Dan Brozoski, Joan Forder, Tom B. Rice, and Hubert V.
Forster from the Medical College of Wisconsin, Milwaukee, WI. Dr. Feroah
will present his team’s findings at the American Physiological Society’s (APS)
(www.the-aps.org)
annual scientific conference, Experimental Biology 2003, being held
April 17-21, 2004, at the Washington, D.C. Convention Center.
Methodology
Research in inbred strains of mice has previously shown
distinct variations in the pattern of slow wave sleep between some strains.
This study investigated differences in circadian slow wave sleep and
activity patterns in three inbred strains of rats previously used in
sequencing the rat genome. If a difference in the pattern of slow wave sleep
and activity was found, then a dissection of the multigenic basis of the
neurophysiological mechanisms involved in the control of slow wave sleep and
behavior could then be explored using consomic (chromosomal substitution)
rat panels.
In Brown Norway (BN/mcw), Dahl Salt Sensitive (SS),
and Fawn Hooded (FH) inbred rats, movement and slow wave sleep were measured
continuously for three days in an environmental controlled chambers in which
temperature and humidity were held within a limited operating range. Slow
wave sleep was determined from electroencephalograph electrodes attached to
the skull and electromyograph electrodes in the neck muscles of the rat.
The percent of slow wave sleep (percent of SWS; SWS bout length relative to
rest time interval), percent of rest (total rest time relative to interval
time) and fragmentation of rest (Frag; calculated as the number of
transitions (per hour) from a minimum six second rest period to a minimum
four second period of activity) was obtained from a computerized open-field
activity monitoring system that was integrated with the sleep system.
Results
Unique and significant differences were found within
and between strains over the study period. The researchers found that the
percentage of slow wave sleep, rest and transitions between rest and
activity varied uniquely between strains. This suggests that these findings
are due to genetic differences. Furthermore, the inverse relationship
between the percentages of slow wave sleep and rest within strains supports
the homeostatic control theory of slow wave sleep, which is to restore
glycogen during non-REM sleep.
Conclusions
The next step in this research is to examine the
consomic rat panels cross of FH and BN that could aid in locating the
chromosome region(s) that are at the very basis of the relationship between
the slow wave sleep and activity. Similarly, examining the consomic rat
panel cross between the SS and FH inbred strains for the chromosomal
region(s) that influence the phase shift in the circadian pattern of slow
wave sleep and activity could also help understand the complex basis of the
early bird and night owl pattern of sleep that is observed in our society.
This research would be important in establishing the
genomic basis of normal and abnormal variation in sleep patterns. Further
research into the genetic basis of these differences may very well help
dissect the multigenic and physiologic mechanistic pathways involved in
circadian sleep and behavior in rats that would be homologous to those in
humans.
- end -
The
American Physiological Society (APS) was founded in 1887 to foster basic and
applied science, much of it relating to human health. The Bethesda, MD-based
Society has more than 11,000 members and publishes 3,800 articles in its 14
peer-reviewed journals every year.
***
Editor’s
Note: For further information or to schedule an interview with a member of
the research team, please contact Donna Krupa at 703.967.2751 (cell),
703.527.7357 (office) or at
djkrupa1@aol.com. Or contact the APS newsroom at 202.249.4009 between
9:00 AM and 6:00 PM EDT April 17-21, 2004.
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