Abstract
BackgroundVariation in circadian rhythms and nocturnality may, hypothetically, be related to or independent of genetic variation in photoperiodic mediation of seasonal changes in physiology and behavior. We hypothesized that strain variation in photoperiodism between photoperiodic F344 rats and nonphotoperiodic Harlan Sprague Dawley (HSD) rats might be caused by underlying variation in clock function. We predicted that HSD rats would have more activity during the day or subjective day, longer free-running rhythms, poor entrainment to short day length, and shorter duration of activity, traits that have been associated with nonphotoperiodism in other laboratory rodent species, relative to F344 rats. An alternative hypothesis, that differences are due to variation in melatonin secretion or responses to melatonin, predicts either no such differences or inconsistent combinations of differences.MethodsWe tested these predictions by examining activity rhythms of young male F344 and HSD rats given access to running wheels in constant dark (DD), short day length (L8:D16; SD), and long day length (L16:D8; LD). We compared nocturnality (the proportion of activity during night or subjective night), duration of activity (alpha), activity onset and offset, phase angle of entrainment, and free running rhythms (tau) of F344 and HSD rats.ResultsHSD rats had significantly greater activity during the day, were sometimes arrhythmic in DD, and had significantly longer tau than F344 rats, consistent with predictions. However, HSD rats had significantly longer alpha than F344 rats and both strains entrained to SD, inconsistent with predictions.ConclusionThe ability of HSD rats to entrain to SD, combined with longer alpha than F344 rats, suggests that the circadian system of HSD rats responds correctly to SD. These data offer best support for the alternative hypothesis, that differences in photoresponsiveness between F344 and HSD rats are caused by non-circadian differences in melatonin secretion or the response to melatonin.
Highlights
Variation in circadian rhythms and nocturnality may, hypothetically, be related to or independent of genetic variation in photoperiodic mediation of seasonal changes in physiology and behavior
Under the hypothesis that differences in clock function cause nonphotoresponsiveness in Harlan Sprague Dawley (HSD) rats, we predicted that HSD rats would be more likely to be arrhythmic or have poorly defined circadian rhythms of activity, because a damaged or altered clock or clock output pathways that result in an inability to track time-of-day or to pass timeof-day information to other areas of the brain would result in poor circadian regulation of activity
If HSD rats were found to be able to entrain activity to the dark period at least in long photoperiod, we predicted a free-running rhythm greater than 24 hours in HSD rats along with inability to lengthen the activity period when moved from long days to short days
Summary
Variation in circadian rhythms and nocturnality may, hypothetically, be related to or independent of genetic variation in photoperiodic mediation of seasonal changes in physiology and behavior. That differences are due to variation in melatonin secretion or responses to melatonin, predicts either no such differences or inconsistent combinations of differences Precise timing of both circadian and seasonal changes in physiology and behavior are important for animals [1]. Genetic variation for circadian clock function can affect circadian physiological rhythms, daily cyclical behaviors, onset and offset of activity, melatonin rhythms, and regulation of seasonal physiological changes in energetics and reproduction [4,5,6] Such genetic variation may affect animal and human health and function through effects on biological rhythms and related physiological systems [4,7,8,9]. It is not clear how commonly variation in photoperiodic seasonality is correlated with circadian rhythms, and additional models that relate genetic variation in circadian and seasonal function would be useful
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