SLEEP 2011 Abstract Supplement

A. Basic Science XI. Sleep Deprivation
an auto-scoring program to start a slowly rotating bar in the animal’s
cage upon detection of sleep onset (Pinnacle Technology, Inc.). During
CPSR, the program was on for 16 hours (Zeitgeber Time (ZT) 8-24) and
off for 8 hours (ZT 0-8). A standard 12:12 light:dark (LD) cycle (lights
on at ZT 0) was used throughout.
Results: The CPSR protocol results in a consistent 25% reduction in total
daily sleep amount. Throughout CPSR, rats fed a high-fat diet maintain
baseline body weight, whereas rats on regular chow exhibit weight
loss (HF: + 0.333 ± 3.37 grams, RC: -27.667 ± 3.07 grams; p < 0.05,
Student’s t-test). Rats on a high-fat diet also consume significantly more
calories during CPSR (average daily caloric intake: baseline = 0.200 ±
0.005 kcal/g BW, CPSR = 0.245 ± 0.003 kcal/g BW; p < 0.001, Student’s
t-test), which was not observed in animals fed regular chow.
Conclusion: A high-fat diet leads to increased caloric intake and prevents
weight loss associated with CPSR in rats, providing an animal
model of CPSR that may more closely reflect the effects of short sleep
in humans.
Support (If Any): This work was supported by NIH 5P01AG011412-14
and NIH 5T32HL007909-13.
0270
MODIFYING SLEEP DURATION REVERSES RELATIONSHIP
BETWEEN BODY WEIGHT AND SLEEP DURATION
Buzzetti R 1 , Hinojosa-Kurtzberg M 1,2 , Shea TJ 3,1 , Ibuki Y 1 , Sirakis GD 1,2 ,
Parthasarathy S 1,2
1
Research Service Line, Southern Arizona VA HealthCare System,
Tucson, AZ, USA, 2 Arizona Respiratory Center, University of Arizona,
Tucson, AZ, USA, 3 University of Arizona, Tucson, AZ, USA
Introduction: In a rodent model of experimental sleep deprivation,
shortening sleep duration has resulted in weight loss, but involved
increased physical activity which may have caused the weight loss.
A recently validated method of sleep interruption can produce gentle
movement of mice by a timed orbital shaker without increased physical
activity. Such a technique facilitates the study of the relationship between
sleep and obesity without the confounding influence of physical
activity. We set out to study the effects of chronic sleep deprivation (21
days) on weight changes in a murine model of sleep deprivation without
the confounding influence of increments in physical activity. A secondary
objective was to study the cross-sectional association between body
weight and sleep duration in a murine model.
Methods: Thirty-three mice (C57Bl/6; JAX, Bar Harbor, ME) were
subjected to either chronic sleep deprivation (n=16) or control condition
(n=17). Sleep deprivation was achieved by placing the mice in cages on
orbital shakers that were gently activated by timers during the light cycle
for 19 days and followed by activation over 24 hours/day for 2 days.
Results: At baseline, before sleep deprivation, EEG-derived sleep efficiency
of mice in the top 50 th percentile of weight (median 55.7%;
IQR, 47.1, 58.4) tended to be lower than that of mice in the bottom 50 th
percentile (median 63.6%; IQR, 56.8, 68.8; P=0.06). Animals subjected
to chronic sleep deprivation without increments in physical activity exhibited
significant weight reduction (-6.4 ± 5.3%) when compared to
animals in the control condition (2.1 ± 4.6%; P500 msec). For each subject, speed and lapses were averaged over the
last 12 hours of TSD (08:00 - 20:00) and last 12 hours of CSR (CSR7;
08:00 - 20:00). A variance components analysis was performed and intraclass
correlation coefficients (ICC) were computed. The same was
calculated for the first 12 hours of the first Recovery Day (R1; 08:00 -
20:00) from both TSD and CSR.
Results: Volunteers responded similarly to TSD and CSR (ICC lapses
= 0.86, p = 0.007; ICC speed = 0.79, p = 0.010) and showed similar
recovery from TSD and CSR (ICC lapses = 0.75, p = 0.013; ICC speed
= 0.89, p = 0.006).
Conclusion: We found strong evidence for trait-like inter-individual
variability in response to TSD and CSR as measured by PVT speed and
lapses: subjects who displayed greater vulnerability to TSD also displayed
greater vulnerability to CSR. These results expand upon previous
findings showing trait-like vulnerability under TSD and show that
such vulnerability extends to other forms of sleep loss including CSR.
The results further suggest that TSD may serve as an assay to predict
individual responsivity to CSR. Analyses are currently underway to determine
the extent to which genetic polymorphisms contribute to this
trait-like vulnerability and to which other measures (e.g., objective and
subjective sleepiness) reveal trait-like inter-individual variability.
Support (If Any): The views expressed in this presentation are those of
the authors and do not reflect the official policy or position of the Walter
Reed Army Institute of Research, the Department of the Army, the
Department of Defense, the U.S. Government, or any institutions with
which the authors are affiliated.
0272
CIRCADIAN CLOCK T3111C POLYMORPHISM
ASSOCIATED WITH INDIVIDUAL DIFFERENCES IN
EXECUTIVE FUNCTIONING, SLEEPINESS AND MOOD
DURING SLEEP RESTRICTION
Goel N 1 , Banks S 1,2 , Lin L 3 , Mignot E 3 , Dinges DF 1
1
Division of Sleep and Chronobiology, Department of Psychiatry,
University of Pennsylvania School of Medicine, Philadelphia, PA,
USA, 2 Centre for Sleep Research, University of South Australia,
Adelaide, SA, Australia, 3 Center for Narcolepsy, Department of
Psychiatry and Behavioral Sciences, and Howard Hughes Medical
Institute, Stanford University, Palo Alto, CA, USA
Introduction: The CLOCK T3111C polymorphism has been reported
to be associated with aspects of sleep, sleepiness, and morningnesseveningness
in healthy adults, and with insomnia in bipolar disorder
and major depressive disorder. We evaluated the CLOCK T3111C polymorphism’s
role in cognitive, sleepiness, sleep homeostatic and mood
responses during baseline and chronic partial sleep deprivation (PSD).
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SLEEP, Volume 34, Abstract Supplement, 2011