|Volume 6 Issue 110 Published - 14:00 UTC 08:00 EST 19-Apr-2004 Next Update - 14:00 UTC 08:00 EST 20-Apr-2004||Editor: Susan K. Boyer, RN
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Animal study finds a link in genetics that determines our sleep patterns
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 2004, being held April 17-21, 2004, at the Washington, D.C. Convention Center.
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.
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.
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.